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

    loading  Checking for direct PDF access through Ovid



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.


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.

Related Topics

    loading  Loading Related Articles