LINC00649 Regulates Endoplasmic Reticulum Stress-mediated Cervical Carcinoma Cell Apoptosis via miR-424-5p/IGF1R Axis
10.3971/j.issn.1000-8578.2022.21.0597
- VernacularTitle:LINC00649通过miR-424-5p/IGF1R轴调控内质网应激介导的宫颈癌细胞凋亡
- Author:
Huiwen DAN
1
;
Huanmin ZHANG
;
Tingting WANG
Author Information
1. Department of Gynaecology and Obstetrics, The 971st Naval Hospital of PLA, Qingdao 266071, China
- Publication Type:Research Article
- Keywords:
LINC00649;
miR-424-5p;
IGF1R;
Cervical carcinoma;
Endoplasmic reticulum stress
- From:
Cancer Research on Prevention and Treatment
2022;49(2):101-109
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effects of LINC00649/miR-424-5p/IGF1R on ERs-mediated apoptosis of cervical carcinoma (CC) cells. Methods CC-related data was obtained from GEO database, then the differentially-expressed miRNAs were analyzed. The bioinformatics database was used to predict the upstream and downstream targets of miR-424-5p. LINC00649 and IGF1R were included. Dual luciferase reporter assay was adopted to confirm the targeting relationship. qRT-PCR was used to detect the expression levels of LINC00649, miR-424-5p and IGF1R in CC tissue and cells. CCK-8 and flow cytometry were used to evaluate the proliferation and apoptosis of CC cells. Western blot was used to detect the expression of ERs-related proteins GRP78, CHOP and Caspase-12. Results Compared with paracancerous tissue and H8 cells, LINC00649 and IGF1R were up-regulated in CC tissue and cells, while miR-424-5p was down-regulated (both P < 0.05). The abnormally high expression of LINC00649 in CC was related to poor prognosis. The knockdown of LINC00649 inhibited CC cell viability and induced cell apoptosis by promoting ERs (all P < 0.05). LINC00649 upregulated the expression of IGF1R via absorbing miR-424-5p. miR-424-5p inhibitor or IGF1R overexpression partially reversed the effects of LINC00649 knockdown on CC cells (both P < 0.05). Conclusion LINC00649 could reduce cell apoptosis and improve cell viability by inhibiting the ERs process via regulating miR-424-5p/IGF1R axis in CC.
