Research Paper Volume 15, Issue 20 pp 11052—11066
The HNF4A-CHPF pathway promotes proliferation and invasion through interactions with MAD1L1 in glioma
- 1 Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
- 2 Science Research Center, East China Institute of Digital Medical Engineering, Shangrao, Jiangxi Province, China
- 3 Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China
- 4 Department of Health Management Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
Received: May 30, 2023 Accepted: August 22, 2023 Published: October 17, 2023
https://doi.org/10.18632/aging.205076How to Cite
Copyright: © 2023 Luo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Chondroitin polymerizing factor (CHPF) is an important glycosyltransferases that participates in the biosynthesis of chondroitin sulfate (CS). Our previous study showed that silencing CHPF expression inhibited glioma cell proliferation in vitro, but the molecular mechanisms by which CHPF contributes to development of glioma have not been characterized. In this study, we found that CHPF was up-regulated in glioma tissues and was positively correlated with malignant clinical pathological characteristics of patients with glioma. Silencing CHPF expression inhibited proliferation, colony formation, migration, and cell cycle of glioma cells. Moreover, silencing CHPF suppressed glioma malignance in vivo. Immunoprecipitation, co-immunoprecipitation, GST pulldown, and liquid chromatography-mass spectrometry (LC-MS/MS) assays were used to verify the interaction between CHPF and Mitotic arrest deficient 1-like 1 (MAD1L1). In addition, Chromatin Immunoprecipitation (ChIP)-PCR analysis showed that HNF4A bound to the CHPF promoter region, which indicated that the transcription factor hepatocyte nuclear factor 4A (HNF4A) could regulate the expression of CHPF in glioma cells.