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Peng Ning Department of Histology and Embryology, Fourth Military Medical University, Xi’an, China
Department of Tumor Radiotherapy, 3rd Hospital of PLA, Bao Ji, China

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Jia-guo Zhong Section 2 of Department of Surgery, 42nd Hospital of PLA, Jiajiang County Leshan City, Sichuan, China

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Fan Jiang Department of Tumor Radiotherapy, 3rd Hospital of PLA, Bao Ji, China

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Yi Zhang Department of Tumor Radiotherapy, 3rd Hospital of PLA, Bao Ji, China

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Jie Zhao Department of Histology and Embryology, Fourth Military Medical University, Xi’an, China

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Feng Tian Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, China

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Wei Li Department of Histology and Embryology, Fourth Military Medical University, Xi’an, China

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Understanding how castration-resistant prostate cancer (CRPC) cells survive the androgen-deprivation condition is crucial for treatment of this advanced prostate cancer (PCa). Here, we reported for the first time the up-regulation of protein S (PROS), an anticoagulant plasma glycoprotein with multiple biological functions, in androgen-insensitive PCa cells and in experimentally induced castration-resistant PCa cells. Overexpression of exogenous PROS in LNCaP cells reduced androgen deprivation-induced apoptosis and enhanced anchorage-dependent clonogenic ability under androgen deprivation condition. Reciprocally, PROS1 knockdown inhibited cell invasiveness and migration, caused the growth inhibition of castration-resistant tumor xenograft under androgen-depleted conditions, and potentiated Taxol (a widely prescribed anti-neoplastic agent)-mediated cell death in PC3 cells. Furthermore, PROS overexpression significantly stimulated AKT activation but failed to evoke oxidative stress in LNCaP cells under normal condition, suggesting that the malignance-promoting effects of the above-mentioned pathway may occur in the order of oxidative stress/PROS/AKT. The potential mechanism may be due to control of oxidative stress-elicited activation of PI3K-AKT-mTOR pathway. Taken together, our gain-of-function, loss-of-function analyses suggest that PROS may facilitate cell proliferation and promote castration resistance in human castration-resistant PCa-like cells via its apoptosis-regulating property. Future study emphasizing on delineating how PROS regulate cellular processes controlling transformation during the development of castration resistance should open new doors for the development of novel therapeutic targets for CRPC.

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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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Qun Liu
Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Hui-ting Dong
Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Tingting Zhao Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Fan Yao Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Yingying Xu Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Bo Chen Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Yunfei Wu Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Feng Jin Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Peng Xing Department of Surgical Oncology, Breast Surgery, General Surgery, First Affiliated Hospital of China Medical University, Shenyang, China

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Cancer-associated adipocytes (CAAs) have been suggested to promote tumor progression. Yet, the role of CAAs in triple-negative breast cancer (TNBC) is poorly investigated. We compared the expression of secretory protein-encoding genes in CAAs and control adipocytes. The effect of key secretory protein(s) on TNBC cell behaviors was explored. CAAs expressed and secreted FUCA2 at greater levels than control adipocytes. When FUCA2 activity was blocked with a neutralizing antibody, TNBC cell proliferation and migration induced by CAA-conditioned medium was impaired. In contrast, supplement of exogenous FUCA2 protein reinforced the proliferation, colony formation, and migration of TNBC cells. In vivo studies confirmed that FUCA2 exposure enhanced tumorigenesis and metastasis of TNBC cells. Mechanistic investigation revealed that FUCA2 induced TNBC aggressiveness through TM9SF3-dependent signaling. Depletion of TM9SF3 blocked CAA- and FUCA2-induced TNBC cell proliferation and migration. Compared to adjacent breast tissues, TNBC tissues had increased expression of TM9SF3. Moreover, high TM9SF3 expression was associated with advanced TNM stage, lymph node metastasis, and shorter overall survival of TNBC patients. Altogether, CAAs secrete FUCA2 to promote TNBC growth and metastasis through interaction with TM9SF3. Inhibition of TM9SF3 may represent a potential therapeutic strategy in the treatment of TNBC.

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