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Bin Li Department of Neurosurgery, Peking University People’s Hospital, Beijing, China

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Sida Zhao Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

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Yiyuan Chen Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

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Hua Gao Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

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Weiyan Xie Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

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Hongyun Wang Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

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Peng Zhao Department of Neurosurgical, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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Chuzhong Li Department of Neurosurgical, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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Yazhuo Zhang Department of Neurosurgical, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

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The clinical diagnosis and treatment of pituitary neuroendocrine tumors (PitNETs) that invade the cavernous sinus are fraught with difficulties and challenges. Exploring the biological characteristics involved in the occurrence and development of PitNETs that invade the cavernous sinus will help to elucidate the mechanism of cavernous sinus invasion. There are differences between intrasellar tumors (IST) and cavernous sinus-invasion tumors (CST) in ultramicrostructure, tumor microenvironment (TME), gene expression, and signaling pathways. The microvascular endothelial cell is increased in CST. The VEGFR signaling pathway, VEGF signaling pathway, and chemokine signaling pathway are activated in CST. HSPB1 is upregulated in CST and promotes cell proliferation, cell viability, and migration. HSPB1 promotes the release of VEGF from GT1-1 cells and activates the VEGF signaling pathway in bEnd.3 cells. HSPB1 promotes the migration of bEnd.3 cells to GT1-1 cells and promotes the formation of blood vessels of bEnd.3 cells. bEnd.3 cells can release CCL3 and CCL4 and promote the vitality, proliferation, and migration of GT1-1 cells. HSPB1 promotes the formation of blood vessels of bEnd.3 cells and ultimately leads to tumor growth in vivo. HSPB1 acts as a key gene for invasion of the cavernous sinus in PitNETs, remodeling TME by promoting the formation of blood vessels of brain microvascular endothelial cells. The synergistic effect of tumor cells and microvascular endothelial cells promotes tumor progression. The mechanism by which HSPB1 promotes tumor invasion by inducing angiogenesis in PitNETs may be a new target for the treatment of PitNETs invading the cavernous sinus.

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Hung-Ming Lam Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Bin Ouyang Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Jing Chen Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Jun Ying Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Jiang Wang Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Chin-Lee Wu Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Li Jia Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Mario Medvedovic Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA
Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Robert L Vessella Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Shuk-Mei Ho Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA
Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA
Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA
Department of Environmental Health, Department of Pathology and Laboratory Medicine, Department of Pathology, Department of Medicine, Center for Environmental Genetics, Department of Urology, Cincinnati Veterans Affairs Medical Center, Cincinnati Cancer Center, University of Cincinnati Medical Center, Room 128 Kettering Complex, Cincinnati, Ohio 45267‐0056, USA

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Castration-resistant prostate cancer (CRPC) is an advanced-stage prostate cancer (PC) associated with high mortality. We reported that G-1, a selective agonist of G protein-coupled receptor 30 (GPR30), inhibited PC cell growth by inducing G2 cell cycle arrest and arrested PC-3 xenograft growth. However, the therapeutic actions of G-1 and their relationships with androgen in vivo are unclear. Using the LNCaP xenograft to model PC growth during the androgen-sensitive (AS) versus the castration-resistant (CR) phase, we found that G-1 inhibited growth of CR but not AS tumors with no observable toxicity to the host. Substantial necrosis (approximately 65%) accompanied by marked intratumoral infiltration of neutrophils was observed only in CR tumors. Global transcriptome profiling of human genes identified 99 differentially expressed genes with ‘interplay between innate and adaptive immune responses’ as the top pathway. Quantitative PCR confirmed upregulation of neutrophil-related chemokines and inflammation-mediated cytokines only in the G-1-treated CR tumors. Expression of murine neutrophil-related cytokines also was elevated in these tumors. GPR30 (GPER1) expression was significantly higher in CR tumors than in AS tumors. In cell-based experiments, androgen repressed GPR30 expression, a response reversible by anti-androgen or siRNA-induced androgen receptor silencing. Finally, in clinical specimens, 80% of CRPC metastases (n=123) expressed a high level of GPR30, whereas only 54% of the primary PCs (n=232) showed high GPR30 expression. Together, these results provide the first evidence, to our knowledge, that GPR30 is an androgen-repressed target and G-1 mediates the anti-tumor effect via neutrophil-infiltration-associated necrosis in CRPC. Additional studies are warranted to firmly establish GPR30 as a therapeutic target in CRPC.

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Shuai Dong The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Jun Pan The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Yi-Bin Shen The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Li-Xian Zhu The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Liang Chen The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Feng Zhu The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Hui Li Zhejiang University, Hangzhou, Zhejiang, China

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Hai-Xiang Shen Zhejiang University, Hangzhou, Zhejiang, China

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Qing Xia People’s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China

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Yi-Jun Wu The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Xiao-Jun Xie The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China

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Thyroid cancer is one of the most common endocrine malignancies. It is necessary to discover more effective molecular targets for the treatment of thyroid cancer. The results of immunohistochemical staining, qPCR and Western blot indicated that the expression of SYT7 in thyroid cancer tissues and cells was higher than that in paracarcinoma tissues and normal thyroid cells. Through cell function testing experiments, it was found that SYT7 knockdown inhibited the proliferation and migration of thyroid cancer cells and promoted cell apoptosis, while SYT7 overexpression had the opposite effect. Similarly, SYT7 downregulation also suppressed tumor growth in vivo. HMGB3 was confirmed to be the downstream gene of SYT7 by GeneChip and Ingenuity Pathway Analysis. Besides, through UbiBrowser database predictions and Co-IP assays, we found that SYT7 interacted with BRCA1 to inhibit HMGB3 ubiquitination and thus upregulated the protein level of HMGB3. Similar to SYT7, HMGB3 was significantly upregulated in thyroid cancer. HMGB3 knockdown inhibited the proliferation and migration of thyroid cancer cells and promoted cell apoptosis. Furthermore, HMGB3 knockdown restored the promotion of cell proliferation and migration caused by SYT7 overexpression. SYT7 and HMGB3 were upregulated in thyroid cancer, and SYT7 regulated the expression of HMGB3 through BRCA1-mediated ubiquitination of HMGB3 to promote thyroid cancer progression.

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Fei Han Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Wen-bin Liu Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Jian-jun Li Department of Oncology, Southwest Hospital, Army Medical University, Chongqing, China

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Ming-qian Zhang Department of Emergency, Yan’an Hospital, Kunming Medical University, Kunming, Yunnan Province, China

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Jun-tang Yang Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Xi Zhang Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Xiang-lin Hao Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Li Yin Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Cheng-yi Mao Department of Pathology, Daping Hospital, Army Medical University, Chongqing, China

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Xiao Jiang Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Jia Cao Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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Jin-yi Liu Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing, China

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New potential biomarkers and therapeutic targets for ovarian cancer should be identified. The amplification in chromosomal region 5q31–5q35.3 exhibits the strongest correlation with overall survival (OS) of ovarian cancer. SOX30 coincidentally located at this chromosomal region has been determined as a new important tumor suppressor. However, the prognostic value, role and mechanism of SOX30 in ovarian cancer are unexplored. Here, we reveal that SOX30 is frequently overexpressed in ovarian cancer tissues and is associated with clinical stage and metastasis of ovarian cancer patients. High SOX30 expression predicts better OS and acts as an independent prognostic factor in advanced-stage patients, but is not associated with OS in early-stage patients. Based on the survival analyses, the advanced-stage patients with high SOX30 expression can receive platin- and/or taxol-based chemotherapy, whereas they should not receive chemotherapy containing gemcitabine or topotecan. Functionally, SOX30 strongly inhibits tumor cell migration and invasion in intro and suppresses tumor metastasis in vivo. SOX30 regulates some markers (E-CADHERIN, FIBRONECTIN, N-CADHERIN and VIMENTIN) and prevents the characteristics of epithelial–mesenchymal transition (EMT). SOX30 transcriptionally regulates the expression of E-CADHERIN, FIBRONECTIN and N-CADHERIN by binding to their promoters. Restoration of E-CADHERIN and/or N-CADHERIN when overexpressing SOX30 significantly reduces the anti-metastatic role of SOX30. Indeed, chemotherapy treatment containing platin or gemcitabine combined with SOX30 expression influences tumor cell metastasis and the survival of nude mice differently, which is closely associated with EMT. In conclusion, SOX30 antagonizes tumor metastasis by preventing EMT process that can be used to predict survival and incorporated into chemotherapeutics of advanced-stage ovarian cancer patients.

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Yulong Li Division of Endocrinology, Department of Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA

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Jianhua Zhang Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

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Poorni R Adikaram Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

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James Welch Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

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Bin Guan Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

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Lee S Weinstein Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

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Haobin Chen Thoracic Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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William F Simonds Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

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Mutation of the CDC73 gene, which encodes parafibromin, has been linked with parathyroid cancer. However, no correlation between genotypes of germline CDC73 mutations and the risk of parathyroid cancer has been known. In this study, subjects with germline CDC73 mutations were identified from the participants of two clinical protocols at National Institutes of Health (Discovery Cohort) and from the literature (Validation Cohort). The relative risk of developing parathyroid cancer was analyzed as a function of CDC73 genotype, and the impact of representative mutations on structure of parafibromin was compared between genotype groups. A total of 419 subjects, 68 in Discovery Cohort and 351 in Validation Cohort, were included. In both cohorts, percentages of CDC73 germline mutations that predicted significant conformational disruption or loss of expression of parafibromin (referred as ‘high-impact mutations’) were significantly higher among the subjects with parathyroid cancers compared to all other subjects. The Kaplan–Meier analysis showed that high-impact mutations were associated with a 6.6-fold higher risk of parathyroid carcinoma compared to low-impact mutations, despite a similar risk of developing primary hyperparathyroidism between two groups. Disruption of the C-terminal domain (CTD) of parafibromin is directly involved in predisposition to parathyroid carcinoma, since only the mutations impacting this domain were associated with an increased risk of parathyroid carcinoma. Structural analysis revealed that a conserved surface structure in the CTD is universally disrupted by the mutations affecting this domain. In conclusion, high-impact germline CDC73 mutations were found to increase risk of parathyroid carcinoma by disrupting the CTD of parafibromin.

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Yu-Xia Chen
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Yan Wang
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Chen-Chun Fu
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Fei Diao
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Liang-Nian Song Department of Pathophysiology, Department of Medicine, the Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, People's Republic of China

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Zong-Bin Li
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Rui Yang
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Jian Lu
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Glucocorticoids (GCs) are widely used as co-medication in the therapy of solid malignant tumors to relieve some of the side effects of chemotherapeutic drugs. However, recent studies have shown that GCs could render cancer cells more resistant to cytotoxic drug-induced apoptosis, but the mechanism is largely unknown. In the present study, we found that the treatment of human ovarian cancer cell lines HO-8910 and SKOV3 with synthetic GCs dexamethasone (Dex) significantly increased their adhesion to extracellular matrix (ECM) and their resistance to apoptosis induced by cytotoxic drugs cisplatin and paclitaxel. Dex also increased the protein levels of adhesion molecules integrins β1, α4, and α5 in HO-8910 cells. The neutralizing antibody against integrin β1 prevented Dex-induced adhesion and significantly abrogated the protective effect of Dex toward cytotoxic agents. We further found that transforming growth factor-β1 (TGF-β1) alone not only increased cell adhesion and cell survival of HO-8910 cells in the presence of cisplatin, but also had synergistic pro-adhesion and pro-survival effects with Dex. Moreover, TGF-β1-neutralizing antibody that could block TGF-β1-induced cell adhesion and apoptosis resistance markedly abrogated the synergistic pro-adhesion and pro-survival effects of Dex and TGF-β1. Finally, we further demonstrated that Dex could up-regulate the expression of TGF-β receptor type II and enhance the responsiveness of cells to TGF-β1. In conclusion, our results indicate that increased adhesion to ECM through the enhancement of integrin β1 signaling and TGF-β1 signaling plays an important role in chemoresistance induced by GCs in ovarian cancer cells.

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Xiao-Hua Jiang Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Jie-Li Lu Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Bin Cui Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Yong-Ju Zhao Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Wei-qing Wang Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Jian-Min Liu Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Wen-Qiang Fang Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Ya-Nan Cao Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Yan Ge Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Chang-xian Zhang Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Huguette Casse Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Xiao-Ying Li Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Guang Ning Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China

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Multiple endocrine neoplasia type 1 (MEN1) is an inherited tumour syndrome characterized by the development of tumours of the parathyroid, anterior pituitary and pancreatic islets, etc. Heterozygous germ line mutations of MEN1 gene are responsible for the onset of MEN1. We investigated the probands and 31 family members from eight unrelated Chinese families associated with MEN1 and identified four novel mutations, namely 373_374ins18, 822delT, 259delT and 1092delC, as well as three previously reported mutations, such as 357_360delCTGT, 427_428delTA and R108X (CGA>TGA) of MEN1 gene. Furthermore, we detected a loss of heterozygosity (LOH) at chromosome 11q in the removed tumours, including gastrinoma, insulinoma and parathyroid adenoma from two probands of MEN1 families. RT-PCR and direct sequencing showed that mutant MEN1 transcripts remained in the MEN1-associated endocrine tumours, whereas normal menin proteins could not be detected in those tumours by either immunohistochemistry or immunoblotting. In conclusion, MEN1 heterozygous mutations are associated with LOH and menin absence, which are present in MEN1-associated endocrine tumours.

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Fei Han Institute of Toxicology, College of Preventive Medicine

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Wen-bin Liu Institute of Toxicology, College of Preventive Medicine

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Jian-jun Li Department of Oncology, Southwest Hospital, Army Medical University, Chongqing, China

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Ming-qian Zhang Department of Emergency, Yan’an Hospital, Kunming Medical University, Kunming, Yunnan Province, China

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Jun-tang Yang Institute of Toxicology, College of Preventive Medicine

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Xi Zhang Institute of Toxicology, College of Preventive Medicine

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Xiang-lin Hao Institute of Toxicology, College of Preventive Medicine

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Li Yin Institute of Toxicology, College of Preventive Medicine

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Cheng-yi Mao Department of Pathology, Daping Hospital, Army Medical University, Chongqing, China

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Xiao Jiang Institute of Toxicology, College of Preventive Medicine

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Jia Cao Institute of Toxicology, College of Preventive Medicine

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Jin-yi Liu Institute of Toxicology, College of Preventive Medicine

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Hongqiang Wang Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China
Department of Oncology, Zhoushan Hospital, Zhoushan, China

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Rui Zhou Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Li Sun Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Jianling Xia Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Xuchun Yang Department of Oncology, Zhoushan Hospital, Zhoushan, China

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Changqie Pan Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Na Huang Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Min Shi Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Jianping Bin Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Yulin Liao Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Wangjun Liao Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Aerobic glycolysis plays an important role in cancer progression. New target genes regulating cancer aerobic glycolysis must be explored to improve patient prognosis. Mitochondrial topoisomerase I (TOP1MT) deficiency suppresses glucose oxidative metabolism but enhances glycolysis in normal cells. Here, we examined the role of TOP1MT in gastric cancer (GC) and attempted to determine the underlying mechanism. Using in vitro and in vivo experiments and analyzing the clinicopathological characteristics of patients with GC, we found that TOP1MT expression was lower in GC samples than in adjacent nonmalignant tissues. TOP1MT knockdown significantly promoted GC migration and invasion in vitro and in vivo. Importantly, TOP1MT silencing increased glucose consumption, lactate production, glucose transporter 1 expression and the epithelial-mesenchymal transition (EMT) in GC. Additionally, regulation of glucose metabolism induced by TOP1MT was significantly associated with lactate dehydrogenase A (LDHA) expression. A retrospective analysis of clinical data from 295 patients with GC demonstrated that low TOP1MT expression was associated with lymph node metastasis, recurrence and high mortality rates. TOP1MT deficiency enhanced glucose aerobic glycolysis by stimulating LDHA to promote GC progression.

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