microRNA-136 inhibits proliferation and promotes apoptosis and radiosensitivity of cervical carcinoma through the NF-κB pathway by targeting E2F1

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Abstract

Aims:

Several microRNAs (miRs) are expressed aberrantly and associated with progression, tumorigenesis, and prognosis of haematological and solid tumors. The study aimed to identify the effects involved with microRNA-136 (miR-136) on the concurrent enhancement of proliferation, apoptosis and radiosensitivity of cervical carcinoma through the NF-κB signaling pathway by targeting E2F1.

Main methods:

Totally 338 patients with cervical carcinoma were recruited in this study. The expressions of miR-136, E2F1, p65, CyclinD1, Atm, Chk2, Bcl-2, Survivin and Bax were detected using RT-qPCR and Western blot analysis. Cells with highest miR-136 expression were subsequently assigned into different groups. Cell survival and apoptosis rate were detected by colony formation assay and flow cytometry, respectively.

Key findings:

Compared to the sensitivity group, E2F1, p65, Bcl-2 and Survivin exhibited increased levels, while expression of CyclinD1, Atm, Chk2, Bax and miR-136 was reduced in the confrontation group. Cell survival rate was declined at 6 and 8 Gy of X-ray irradiation compared with 0, 2 and 4 Gy. Compared with the blank and NC groups, expression of E2F1, p65, Bcl-2 and Survivin was increased, while that of CyclinD1, Atm, Chk2, Bax and miR-136 was all decreased. The cell survival rate was increased; while apoptosis rate was decreased in the miR-136 inhibitor group. The trends observed in the miR-136 mimics and siRNA-E2F1 groups were contradictory to the miR-136 inhibitor group.

Significance:

Based on our results, miR-136 inhibits proliferation, while acting to promote apoptosis and radiosensitivity in cervical carcinoma by targeting E2F1 through the NF-κB signaling pathway, resulting in improved prognoses.

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