Xia Dandan, Xu Xun, Wei Jing, Wang Wenli, Xiong Jiali, Tan Qingqing, Xue Pingping, Wang Huiyan
Department of Obstetrics and Gynecology, Changzhou Maternal and Child Health Care Hospital, Changzhou Medical Center, Nanjing Medical University, Changzhou, 213000, China.
Department of Orthopedics, Changzhou Maternal and Child Health Care Hospital, Changzhou Medical Center, Nanjing Medical University, Changzhou, 213000, China.
Biochem Biophys Rep. 2023 Jul 31;35:101522. doi: 10.1016/j.bbrep.2023.101522. eCollection 2023 Sep.
The molecular mechanism of chromatin assembly factor 1 unit A (CHAF1A) promoting the proliferation and growth of epithelial ovarian cancer (EOC) cells hasn't been reported at present. In this study, recombinant CHAF1A siRNA/overexpression plasmid (si-RNA1/pcDNA3.1-CHAF1A) was designed and constructed, and stable cell lines with knockdown or overexpression of CHAF1A were constructed. The changes of JAK2/STAT3 pathway were detected by Western blot. JAK2/STAT3 pathway was inhibited by Peficitinib, and then cell proliferation and growth ability were detected. Bioinformatics analysis suggested that CHAF1A was up-regulated in epithelial ovarian cancer. JAK2/STAT3 pathway phosphorylation was inhibited in si-RNA1 group, while it was increased in pcDNA3.1-CHAF1A group. After inhibiting JAK2/STAT3 pathway, the promoting effect of CHAF1A on epithelial ovarian cancer cell proliferation disappeared, meanwhile the inhibitory effect of CHAF1A on apoptosis enhanced. In conclusion, CHAF1A promotes the proliferation and growth of epithelial ovarian cancer cells by affecting the phosphorylation of JAK2/STAT3 signaling pathway.
目前,染色质组装因子1亚基A(CHAF1A)促进上皮性卵巢癌(EOC)细胞增殖和生长的分子机制尚未见报道。本研究设计并构建了重组CHAF1A siRNA/过表达质粒(si-RNA1/pcDNA3.1-CHAF1A),构建了CHAF1A基因敲低或过表达的稳定细胞系。采用蛋白质免疫印迹法检测JAK2/STAT3信号通路的变化。用培非替尼抑制JAK2/STAT3信号通路,然后检测细胞增殖和生长能力。生物信息学分析提示CHAF1A在上皮性卵巢癌中呈上调表达。si-RNA1组JAK2/STAT3信号通路磷酸化受到抑制,而pcDNA3.1-CHAF1A组则增强。抑制JAK2/STAT3信号通路后,CHAF1A对上皮性卵巢癌细胞增殖的促进作用消失,同时CHAF1A对细胞凋亡的抑制作用增强。综上所述,CHAF1A通过影响JAK2/STAT3信号通路的磷酸化促进上皮性卵巢癌细胞的增殖和生长。