CHAF1A promotes the proliferation and growth of epithelial ovarian cancer cells by affecting the phosphorylation of JAK2/STAT3 signaling pathway

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 constructe...

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Veröffentlicht in:Biochemistry and biophysics reports 2023-09, Vol.35, p.101522-101522, Article 101522
Hauptverfasser: Xia, Dandan, Xu, Xun, Wei, Jing, Wang, Wenli, Xiong, Jiali, Tan, Qingqing, Xue, Pingping, Wang, Huiyan
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Sprache:eng
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Zusammenfassung: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. •CHAF1A can activate the phosphorylation of JAK2/STAT3 signaling pathway.•Inhibition of JAK2/STAT3 signaling pathway could reduce the effect of CHAF1A overexpression on the proliferation and growth of epithelial ovarian cancer cells.
ISSN:2405-5808
2405-5808
DOI:10.1016/j.bbrep.2023.101522