Department of Oncology, Affiliated Cancer Hospital of Zhengzhou University Henan Cancer Hospital, Zhengzhou, NO. 127, Dongming Road, Jinshui District, Zhengzhou, 450008, Henan, China.
Department of Pathology, Affiliated Cancer Hospital of Zhengzhou University Henan Cancer Hospital, Zhengzhou, 450008, Henan, China.
BMC Mol Cell Biol. 2019 Dec 27;20(1):61. doi: 10.1186/s12860-019-0245-9.
PAX8 was not only a mitotic factor, but identified as a transcription factor involved in the prognosis of human tumor patients. Elucidating the function of PAX8 on the pathology of stomach cancer was meaningful.
PAX8 was found to be upregulated in primary stomach cancer tissue and the TCGA stomach cancer dataset. Interestingly, SOX13 and PAX8 showed consistent expression patterns, and the combined high PAX8 and SOX18 expression induced a worse prognosis of stomach cancer patients. SOX13 was further identified as a transcription factor of PAX8, and further affect Aurora B and Cyclin B1 expression, two cell cycle related factors of the downstream of PAX8, including. Furthermore, PAX8 depletion inducted G1-phase arrest and the decrease of EdU incorporation, cell viability and colony formation can be rescued by SOX13 overexpression.
SOX13 participated in the elevated expression of PAX8, which promote the proliferation of stomach cancer cells. Therefore, SOX13 mediated PAX8 expression was recognized as a tumor-promoting role in stomach cancer.
PAX8 不仅是有丝分裂因子，而且被鉴定为参与人类肿瘤患者预后的转录因子。阐明 PAX8 在胃癌病理中的功能具有重要意义。
PAX8 在原发性胃癌组织和 TCGA 胃癌数据库中均上调。有趣的是，SOX13 和 PAX8 的表达模式一致，高表达 PAX8 和 SOX18 联合诱导胃癌患者预后不良。SOX13 进一步被鉴定为 PAX8 的转录因子，并进一步影响下游的 Aurora B 和 Cyclin B1 表达，这两个是细胞周期相关因子。此外，PAX8 耗竭诱导 G1 期停滞，EdU 掺入减少，SOX13 过表达可挽救细胞活力和集落形成的减少。
SOX13 参与了 PAX8 的上调表达，促进了胃癌细胞的增殖。因此，SOX13 介导的 PAX8 表达被认为在胃癌中具有促进肿瘤的作用。
