miR-133a-5p Inhibits Glioma Cell Proliferation by Regulating IGFBP3

Xinzhi Yang; Dong Chen; Jiliang Hu; Qingsuo Zhao; Xing Fu; Wen Lv

doi:10.1155/2022/8697676

miR-133a-5p Inhibits Glioma Cell Proliferation by Regulating IGFBP3

J Oncol. 2022 Aug 2:2022:8697676. doi: 10.1155/2022/8697676. eCollection 2022.

Authors

Xinzhi Yang¹, Dong Chen², Jiliang Hu^{3

4}, Qingsuo Zhao², Xing Fu⁵, Wen Lv^{3

6}

Affiliations

¹ Department of Neurosurgery, Shenzhen Hospital of Southern Medical University, Shenzhen, Guangdong, China.
² Department of Neurosurgery, Shenzhen Yantian District s People s Hospital, Shenzhen, Guangdong, China.
³ Department of Neurosurgery, Shenzhen People's Hospital, Shenzhen, Guangdong, China.
⁴ Guangdong Engineering Technological Research Center for Nervous Anatomy and Related Clinical Applications, Zhongshan, China.
⁵ Department of Neurosurgery, Changsha Central Hospital of University of South China, Changsha, Hunan, China.
⁶ Department of Neurosurgery, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.

Abstract

Objective: This research aims to investigate the expression of miR-133a-5p in glioma tissues and its impact on glioma cell proliferation.

Methods: Fluorescence-quantitative PCR was used to detect the expression of miR-133a-5p in 25 cases of glioma and adjuncent tissues. CCK-8 and colony formation analyses were used to evaluate the impact of transfection with miR-133a-5p inhibitors or mimics on glioma cell growth and colony formation. The IGFBP3 (insulin-like growth factor-binding protein-3) and miR-133a-5p binding sites were predicted using Starbase, and the miR-133a-5p binding capacity with 3'UTR of IGFBP3 gene was determined using a luciferase gene reporter system. Following transfection with miR-133a-5p mimics or inhibitors, the IGFBP3 protein expression in glioma cells was determined by western blotting. The colony formation assay was applied to evaluate the influence of IGFBP3 overexpression on the miR-133a-5p in glioma cell proliferation. For assessment of the IGFBP3 expression in glioma tissues and prognosis, TCGA database was employed.

Results: The expression of miR-133a-5p was considerably reduced in glioma tissue compared to adjuncent control tissue. In addition, miR-133a-5p expression decreased with increasing glioma malignancy. Glioma cell growth and colony formation were reduced after miR-133a-5p mimics were transfected, while transfection of miR-133a-5p inhibitors had a reverse impact. The expression of IGFBP3 was affected by miR-133a-5p by binding to its 3'UTR region. Additional study demonstrated that the overall survival (OS) of subjects with increased IGFBP3 expression was considerably lower compared to patients with decreased IGFBP3 expression. The IGFBP3 overexpression effectively counteracts the glioma cell proliferation-inhibiting impact of miR-133a-5p.

Conclusion: miR-133a-5p acts as a glioma tumor suppressor gene. It reduces glioma cell proliferation by modulating IGFBP3 and could be a target for glioma therapy.