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Dingwen Liu Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Liang Zhou Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Cheng Li Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Youyou Li Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Jiahao Liu Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Lei Zhou Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Jin Tang Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Wei Xiong Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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Long Wang Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

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This study provides a comprehensive analysis of global, continental, and national trends in the prevalence and mortality of prostate cancer (PC), breast cancer (BC), and thyroid cancer (TC). Utilizing 2021 Global Burden of Diseases (GBD2021) data, prevalence and death rates for 2021 were examined, with temporal trends from 1990 to 2021 analyzed via Joinpoint regression. Annual percentage change (APC) and average APC (AAPC) were calculated with 95% CI. Distributive inequalities were quantified using the slope index of inequality and concentration index. In 2021, PC, BC, and TC showed higher global age-standardized prevalence rates (ASPR) in Europe and America compared to Africa and Asia, while higher age-standardized death rates (ASDR) for PC and BC were noted in Africa. Over the study period, significant global increases in ASPR were observed for PC (AAPC = 0.78, 95% CI: 0.67 to 0.89), BC (AAPC = 0.31, 95% CI: 0.24 to 0.37), and TC (AAPC = 1.42, 95% CI: 1.31 to 1.52). Conversely, ASDR significantly decreased for PC (AAPC = −0.83, 95% CI: −0.92 to −0.74), BC (AAPC = −0.48, 95% CI: −0.56 to −0.39), and TC (AAPC = −0.23, 95% CI: −0.29 to −0.17). Variations were observed across continents and time periods, affecting 204 countries and territories. Higher Social Development Index (SDI) levels were associated with a more pronounced burden of these cancers. The findings highlight significant global heterogeneity in prevalence, death rates, and temporal trends of endocrine cancers, with important implications for epidemiology and public health policies.

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Zhi Long Department of Urology, Third Xiangya Hospital, Institute of Prostate Disease, Central South University, Changsha, China
Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada

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Yinan Li Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada

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Yu Gan Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada
Department of Urology, Xiangya Hospital, Central South University, Changsha, China

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Dongyu Zhao Center for Bioinformatics and Computational Biology, Houston Methodist Research Institute, Houston, Texas, USA
Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, New York, USA
Institute for Academic Medicine, Houston Methodist Hospital, Houston, Texas, USA

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Guangyu Wang Center for Bioinformatics and Computational Biology, Houston Methodist Research Institute, Houston, Texas, USA
Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, New York, USA
Institute for Academic Medicine, Houston Methodist Hospital, Houston, Texas, USA

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Ning Xie Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada

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Jessica M Lovnicki Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada

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Ladan Fazli Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada

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Qi Cao Department of Urology and Robert H. Lurie Comprehensive Cancer Cancer, Northwestern University Reinberg School of Medicine, Chicago, Illinois, USA

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Kaifu Chen Center for Bioinformatics and Computational Biology, Houston Methodist Research Institute, Houston, Texas, USA
Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, New York, USA
Institute for Academic Medicine, Houston Methodist Hospital, Houston, Texas, USA

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Xuesen Dong Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada

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Homeobox A10 (HOXA10) is an important transcription factor that regulates the development of the prostate gland. However, it remains unknown whether it modulates prostate cancer (PCa) progression into castrate-resistant stages. In this study, we have applied RNA in situ hybridization assays to demonstrate that downregulation of HOXA10 expression is associated with castrate-resistant PCa. These findings are supported by public RNA-seq data showing that reduced HOXA10 expression is correlated with poor patient survival. We show that HOXA10 suppresses PCa cell proliferation, anchorage colony formation and xenograft growth independent to androgens. Using AmpliSeq transcriptome sequencing, we have found that gene groups associated with lipid metabolism and androgen receptor (AR) signaling are enriched in the HOXA10 transcriptome. Furthermore, we demonstrate that HOXA10 suppresses the transcription of the fatty acid synthase (FASN) gene by forming a protein complex with AR and prevents AR recruitment to the FASN gene promoter. These results lead us to conclude that downregulation of HOXA10 gene expression may enhance lipogenesis to promote PCa cell growth and tumor progression to castrate-resistant stage.

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Jing Nie Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China
Nanfang Neurosurgery Research Institution, Nanfang hospital, Southern Medical University, Guangzhou, China

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Guang-long Huang Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China
Nanfang Neurosurgery Research Institution, Nanfang hospital, Southern Medical University, Guangzhou, China

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Sheng-Ze Deng Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Yun Bao Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Ya-Wei Liu Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China
Nanfang Neurosurgery Research Institution, Nanfang hospital, Southern Medical University, Guangzhou, China

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Zhan-Peng Feng Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Chao-Hu Wang Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Ming Chen Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China

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Song-Tao Qi Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China
Nanfang Neurosurgery Research Institution, Nanfang hospital, Southern Medical University, Guangzhou, China

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Jun Pan Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China
Nanfang Neurosurgery Research Institution, Nanfang hospital, Southern Medical University, Guangzhou, China

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Craniopharyngiomas (CPs) are usually benign, non-metastasizing embryonic malformations originating from the sellar area. They are, however, locally invasive and generate adherent interfaces with the surrounding brain parenchyma. Previous studies have shown the tumor microenvironment is characterized by a local abundance of adenosine triphosphate (ATP), infiltration of leukocytes and elevated levels of pro-inflammatory cytokines that are thought to be responsible, at least in part, for the local invasion. Here, we examine whether ATP, via the P2X7R, participates in the regulation of cytokine expression in CPs. The expression of P2X7R and pro-inflammatory cytokines were measured at the RNA and protein levels both in tumor samples and in primary cultured tumor cells. Furthermore, cytokine modulation was measured after manipulating P2X7R in cultured tumor cells by siRNA-mediated knockdown, as well as pharmacologically by using selective agonists and antagonists. The following results were observed. A number of cytokines, in particular IL-6, IL-8 and MCP-1, were elevated in patient plasma, tumor tissue and cultured tumor cells. P2X7R was expressed in tumor tissue as well as in cultured tumor cells. RNA expression as measured in 48 resected tumors was positively correlated with the RNA levels of IL-6, IL-8 and MCP-1 in tumors. Furthermore, knockdown of P2X7R in primary tumor cultures reduced, and stimulation of P2XR7 by a specific agonist enhanced the expression of these cytokines. This latter stimulation involved a Ca2+-dependent mechanism and could be counteracted by the addition of an antagonist. In conclusion, the results suggest that P2X7R may promote IL-6, IL-8 and MCP-1 production and secretion and contribute to the invasion and adhesion of CPs to the surrounding tissue.

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