RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway.
10.1007/s11684-022-0929-y
- Author:
Chaochao WANG
1
;
Hao XUE
1
;
Rongrong ZHAO
1
;
Zhongzheng SUN
2
;
Xiao GAO
1
;
Yanhua QI
1
;
Huizhi WANG
1
;
Jianye XU
1
;
Lin DENG
3
;
Gang LI
4
Author Information
1. Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China.
2. Shandong Key Laboratory of Brain Function Remodeling, Jinan, 250012, China.
3. Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China. denglinqilu@163.com.
4. Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, China. dr.ligang@sdu.edu.cn.
- Publication Type:Journal Article
- Keywords:
RGS16;
glioma;
let-7c-5p;
migration;
proliferation
- MeSH:
Humans;
Phosphatidylinositol 3-Kinases/metabolism*;
Proto-Oncogene Proteins c-akt/metabolism*;
MicroRNAs/metabolism*;
Glioma/genetics*;
Genes, Tumor Suppressor;
Cell Proliferation;
Gene Expression Regulation, Neoplastic;
Cell Line, Tumor
- From:
Frontiers of Medicine
2023;17(1):143-155
- CountryChina
- Language:English
-
Abstract:
Gliomas are the most common central nervous system tumours; they are highly aggressive and have a poor prognosis. RGS16 belongs to the regulator of G-protein signalling (RGS) protein family, which plays an important role in promoting various cancers, such as breast cancer, pancreatic cancer, and colorectal cancer. Moreover, previous studies confirmed that let-7c-5p, a well-known microRNA, can act as a tumour suppressor to regulate the progression of various tumours by inhibiting the expression of its target genes. However, whether RGS16 can promote the progression of glioma and whether it is regulated by miR let-7c-5p are still unknown. Here, we confirmed that RGS16 is upregulated in glioma tissues and that high expression of RGS16 is associated with poor survival. Ectopic deletion of RGS16 significantly suppressed glioma cell proliferation and migration both in vitro and in vivo. Moreover, RGS16 was validated as a direct target gene of miR let-7c-5p. The overexpression of miR let-7c-5p obviously downregulated the expression of RGS16, and knocking down miR let-7c-5p had the opposite effect. Thus, we suggest that the suppression of RGS16 by miR let-7c-5p can promote glioma progression and may serve as a potential prognostic biomarker and therapeutic target in glioma.
