Cui Ying, Shen Guihua, Zhou Dan, Wu Fengli
Department of Gynecology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing City 100730, People's Republic of China.
Cancer Manag Res. 2020 Jan 22;12:523-529. doi: 10.2147/CMAR.S226801. eCollection 2020.
It is known that CASC11 can promote colorectal cancer. However, the function of CASC11 in ovarian carcinoma (OC) remains elusive.
In this study, we measured the expression levels of CASC11 and miR-182 in both OC and healthy control samples by performing qPCR. The interaction between CASC11 and miR-182 was analyzed by the overexpression experiment and qPCR. Cell apoptosis was analyzed by cell apoptosis assay, and the prognostic value of CASC11 for OC was analyzed by survival curve analysis.
We found that CASC11 and microRNA-182 (miRNA-182) were upregulated in OC. Plasma CASC11 was upregulated in OC patients and predicted early-stage OC. Follow-up study revealed that high plasma levels of CASC11 were closely correlated with poor survival conditions of OC patients. CASC11 and miRNA-182 were positively correlated in OC. Overexpression of CASC11 mediated the upregulation of miRNA-182 in cells of OC cell lines, while miRNA-182 overexpression did not significantly affect CASC11 expression. Overexpression of CASC11 and miRNA-182 promoted cancer cell proliferation and inhibited cancer cell apoptosis.
Therefore, CASC11 overexpression predicts poor prognosis and CASC11 regulates cell proliferation and apoptosis as well as microRNA-182 expression in ovarian carcinoma.
已知CASC11可促进结直肠癌。然而,CASC11在卵巢癌(OC)中的功能仍不清楚。
在本研究中,我们通过进行qPCR测量了OC样本和健康对照样本中CASC11和miR-182的表达水平。通过过表达实验和qPCR分析CASC11与miR-182之间的相互作用。通过细胞凋亡检测分析细胞凋亡,并通过生存曲线分析分析CASC11对OC的预后价值。
我们发现OC中CASC11和微小RNA-182(miRNA-182)上调。OC患者血浆CASC11上调,并可预测早期OC。随访研究表明,血浆CASC11水平高与OC患者的不良生存状况密切相关。OC中CASC11与miRNA-182呈正相关。CASC11的过表达介导了OC细胞系细胞中miRNA-182的上调,而miRNA-182的过表达对CASC11表达没有显著影响。CASC11和miRNA-182的过表达促进癌细胞增殖并抑制癌细胞凋亡。
因此,CASC11过表达预示预后不良,且CASC11在卵巢癌中调节细胞增殖、凋亡以及微小RNA-182的表达。