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.
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.
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).
Using 98 formalin-fixed, paraffin-embedded samples obtained from patients with esophageal cancer who had received preoperative chemotherapy followed by surgery, we measured expression levels of several miRNAs that are considered to be involved in the regulation of stem cell function (e.g., let-7a, let-7g, miR-21, miR-134, miR-145, miR-155, miR-200c, miR-203, and miR-296) by real-time reverse transcriptase PCR.