miR-885-3p regulates radiosensitivity of colorectal cancer cell HT-29 by targeting AKT1
10.3760/cma.j.issn.0254-5098.2018.12.003
- VernacularTitle:miR-885-3p靶向AKT1对结直肠癌细胞HT-29放射敏感性的影响
- Author:
Quanying LI
1
;
Dapeng WU
;
Hao GU
;
Zhikuan HE
;
Yang WANG
;
Zheng GE
;
Changjiang QIN
;
Wei WANG
Author Information
1. 河南大学淮河医院普通外科
- Keywords:
Colorectal cancer;
miR-885-3p;
Radiosensitivity;
AKT1
- From:
Chinese Journal of Radiological Medicine and Protection
2018;38(12):899-906
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of miR-885-3p on the radiosensitivity of colorectal cancer cell HT-29. Methods The expression of miR-885-3p in HT-29 cells irradiated with different doses (0, 2, 4, 6, 8 Gy) of X-rays was detected by qPCR. The effect of miR-885-3p in modulating cell radiosensitivity was assessed in HT-29 cells with miR-885-3p overexpression. Bioinformatics prediction and dual luciferase reporter gene assay were employed to identify the direct target gene of miR-885-3p. Relationship between miR-885-3p and target gene tyrosine kinase 1 (AKT1) was investigated via regulation of miR-885-3p expression. The effect of AKT1 on radiosensitivity in HT-29 cells was evaluated through knockdown AKT1. The effect of AKT1 on miR-885-3p-induced radiosensitivity was detected by co-transferring miR-885-3p and AKT1 gene into HT-29 cells. Results miR-885-3p expression was up-regulated in radiation-induced HT-29 cells (F=46. 64, P<0. 05). Over-expression of miR-885-3p and knockdown of AKT1 enhanced cell radiosensitization by inhibiting survival and promoting apoptosis (t=12. 33, 12. 95, P <0. 05) with SER of 1. 602 and 1. 946, respectively. Inhibition of miR-885-3p promoted radioresistance by increasing cell survival and inhibiting apoptosis (t=11. 94, P<0. 05) with a SER of 0. 839. AKT1 is a target gene downstream of miR-885-3p, overexpression of AKT1 reversed the effect of miR-885-3p on cell radiosensitivity with a SER of 0. 680. Conclusions miR-885-3p can enhance the radiosensitivity of colorectal cancer HT-29 cells by directly targeting AKT1, which provides a target for improving the radiosensitivity of clinical colorectal cancer.
