细胞分裂周期相关蛋白8通过调节细胞周期和P53/Rb信号通路促进子宫内膜癌细胞的生长并抑制其凋亡。
Cell division cycle associated 8 promotes the growth and inhibits the apoptosis of endometrial cancer cells by regulating cell cycle and P53/Rb signaling pathway.
作者信息
Li Wenxue, Qin Yujing, Chen Xiujuan, Wang Xiaolei
机构信息
Department of Obstetrics and Gynecology, The Affiliated Weihai Second Municipal Hospital of Qingdao University Weihai 264200, Shandong, China.
出版信息
Am J Transl Res. 2023 Jun 15;15(6):3864-3881. eCollection 2023.
OBJECTIVE
Cell division cycle associated 8 (CDCA8) is over-expressed in a variety of tumors and associated with tumor progression. Nevertheless, the role of CDCA8 in endometrial cancer (EC) is unclear. Therefore, this study aimed to assess the role and mechanism of CDCA8 in EC.
METHODS
Immunohistochemical staining was used to evaluate CDCA8 expression in EC, and its relationship with clinicopathology was analyzed. CDCA8 was knocked down or over-expressed to study its effects on cell biological behaviors. Furthermore, the feasible mechanisms of CDCA8 were examined by Western blot.
RESULTS
CDCA8 was significantly upregulated in EC tissue (P<0.05) and related to worse tumor grade, Figo stage, tumor (T) stage, and deep myometrial invasion (P<0.05). CDCA8 knockdown inhibited EC cell activities, promoted apoptosis and induced cell cycle arrest (P<0.05), which were reversed by CDCA8 over-expression (P<0.05). Besides, CDCA8 knockdown inhibited the growth of xenograft tumors in nude mice (P<0.05). Furthermore, CDCA8 may affect cell cycle and P53/Rb signaling pathway in EC cells.
CONCLUSION
CDCA8 plays a role in the pathogenesis of EC and may be a target for EC treatment.
目的
细胞分裂周期相关8（CDCA8）在多种肿瘤中过度表达，并与肿瘤进展相关。然而，CDCA8在子宫内膜癌（EC）中的作用尚不清楚。因此，本研究旨在评估CDCA8在EC中的作用及机制。
方法
采用免疫组织化学染色评估CDCA8在EC中的表达，并分析其与临床病理特征的关系。通过敲低或过表达CDCA8来研究其对细胞生物学行为的影响。此外，通过蛋白质印迹法检测CDCA8的可能作用机制。
结果
CDCA8在EC组织中显著上调（P<0.05），并与较差的肿瘤分级、国际妇产科联盟（FIGO）分期、肿瘤（T）分期及肌层浸润深度相关（P<0.05）。敲低CDCA8可抑制EC细胞活性，促进细胞凋亡并诱导细胞周期阻滞（P<0.05），而过表达CDCA8可逆转上述作用（P<0.05）。此外，敲低CDCA8可抑制裸鼠移植瘤的生长（P<0.05）。进一步研究发现，CDCA8可能影响EC细胞的细胞周期及P53/Rb信号通路。
结论
CDCA8在EC发病机制中起作用，可能成为EC治疗的靶点。
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