These results showed that CCAT2 promoted the radiotherapy resistance of EC cells via negative regulation of the miR‑145/p70S6K1 and the p53 signaling pathways and associated elements may be potential targets for improving the sensitivity of EC radiotherapy.
We observed that lncRNA PVT1 was robustly induced in EC. lncRNA PVT1 could bind to miR-145 and regulate its expression, and FSCN1 is a target gene of miR-145.
In addition, the risk-score model -0.0053*log<sub>2</sub>(<i>CADM2</i>)+0.0168*log<sub>2</sub>(<i>SERPINE1</i>)-0.0073*log<sub>2</sub>(ADAMTS9-AS2)+0.0905*log<sub>2</sub>(PVT1)+0.0047*log<sub>2</sub>(hsa-miR372)-0.0193*log<sub>2</sub>(hsa-miR145), (log<sub>2</sub>[gene count]) could improve diagnosis of EC with an AUC of 0.988.
Expression levels of miR-145 and the marker protein enhanced green fluorescent protein (EGFP) in infected ECA109 and EC9706 human esophageal carcinoma cells were detected by quantitative PCR and flow cytometry, respectively.
Compared to the control group, the expression level of miR-145 in the transfected group was significantly higher (185-fold, P < 0.05). miR-145 overexpression significantly inhibited esophageal cancer cell proliferation (P < 0.05).