This study aims to explore the effects of microRNA-21 (miR-21) on radiosensitivity in non-small cell lung cancer (NSCLC) by targeting programmed cell deanth 4 (PDCD4) and regulating PI3K/AKT/mTOR signaling pathway. Cancer tissues and adjacent normal tissues were collected from 97 NSCLC patients who received a standard radiotherapy regimen. TUNEL assay was applied to determine cell apoptosis in tissues. The qRT-PCR assay was used to detect the expressions of miR-21 expression and PDCD4 mRNA. The protein expressions of PDCD4 and PI3K/AKT/mTOR signaling pathway-related proteins were determined by Western blotting. Colony formation assay was used to observe the sensitivity to radiotherapy of NSCLC cells. Flow cytometry was adopted to testify cell apoptosis. Compared with adjacent normal tissues, miR-21 expression was significantly increased and the mRNA and protein expressions of PDCD4 were decreased in NSCLC tissues. Higher miR-21 expression was associated with attenuated radiation efficacy and shorter median survival time. PDCD4 was the target gene of miR-21. The miR-21 mimics and siRNA-PDCD4 decreased the sensitivity to radiotherapy and cell apoptosis of A549 and H1299 cells and activated PI3K/AKT/mTOR pathway. The sensitivity of A549 and H1299 cells was strengthened in the miR-21 inhibitors group and the PI3K/AKT/mTOR inhibitors group. The siRNA-PDCD4 could reverse the effects of miR-21 inhibitors on sensitivity to radiotherapy and cell apoptosis of NSCLC cells. Our findings provide strong evidence that miR-21 could inhibit PDCD4 expression and activate PI3K/AKT/mTOR signaling pathway, thereby affecting the radiation sensitivity of NSCLC cells.

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This study aims to explore how microRNA-133a (miR-133a) affects cell apoptosis and radio-sensitivity by targeting EGFR via regulating MEK/ERK pathway in esophageal cancer (EC). A total of 358 EC patients were selected and assigned into the resistant and sensitive groups. Human EC KYSE 150 cell line was assigned into the blank, negative control (NC), miR-133a mimic, miR-133a inhibitors, si-EGFR, miR-133a inhibitors + si-EGFR groups after transfection. MiR-133a and EGFR mRNA expressions were detected by qRT-PCR and EGFR, MEK/ERK pathway-related protein expressions were detected by Western blotting. The radio-sensitivity and cell apoptosis were testified by clone formation and flow cytometry. MiR-133a was up-regulated but EGFR was down-regulated in the sensitive group than in the resistant group. Compared with the blank and NC groups, the miR-133a mimic and si-EGFR groups exhibited increased cell apoptosis rate but decreased EGFR, p-MEK1/2, and p-ERK1/2 protein expressions; while opposite trend was observed in the miR-133a inhibitors group. Compared with the miR-133a inhibitors group, the miR-133a inhibitors + si-EGFR group presented reduced cell survival rate, EGFR, p-MEK1/2, and p-ERK1/2 protein expressions but increased cell apoptosis rate. These results indicated that miR-133a could inhibit the MEK/ERK pathway to promote cell apoptosis and enhance radio-sensitivity by targeting EGFR in EC. J. Cell. Biochem. 118: 2625-2634, 2017. © 2017 Wiley Periodicals, Inc.

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