MiR-646 inhibited cell proliferation and migration by targeting P62 in glioma

MiR-646, a small non-coding RNA, poorly expressed in a variety of tumors. This study aimed to clarify the role of miR-646 and its underlying mechanisms in glioblastoma (GBM). In our study, we found that miR-646 mRNA levels were lower in tumor tissues than in non-cancer tissues. The ability of glioma...

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Bibliographic Details
Main Authors: Fangyu Ye, Heng Zhang, Qianqian Chen, Yanping Gui, Geng Tian, Yuting Ye, Xin Chen, Haijuan Dong, Xiangshan Fan, Jun Chen, RuiYing Yuan, Li Zhao, Juping Yu
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Cell Adhesion & Migration
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Online Access:https://www.tandfonline.com/doi/10.1080/19336918.2025.2515763
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Summary:MiR-646, a small non-coding RNA, poorly expressed in a variety of tumors. This study aimed to clarify the role of miR-646 and its underlying mechanisms in glioblastoma (GBM). In our study, we found that miR-646 mRNA levels were lower in tumor tissues than in non-cancer tissues. The ability of glioma cells to proliferate, invade, and migrate is diminished by miR-646 overexpression in vitro and in vivo. Mechanistically, miR-646 targeted sequestosome 1 (p62) in the 3’UTR and affected the Keap1/Nrf2 pathway, thus attenuating the expression of the HO-1 gene. In conclusion, this study provided a novel finding that miR-646 tampered with gliomagenesis by regulating the p62/Keap1/Nrf2 axis, which provides a potential target for GBM therapy.
ISSN:1933-6918
1933-6926