CircUGP2 inhibits tumor progression via PI3K/AKT/mTOR signaling through sponging miR-137-3p and interacting with UPF1 in hepatocellular carcinoma.

Authors

Longfei Xie, Suxin Li, Huahu Guo, Wenhui Zhang, Mengjie Shang, Bailin Cheng, Dingyang Li, Luhao Li, Zhaochen Liu, Lin Li, Liang Bao, Kaiwei Tian, Chengxuan Li, Xiaowei Dang

Published in

Frontiers in immunology. Volume 17. Pages 1926747. Epub Oct 02, 2026.

Abstract

Circular RNA (circRNA) has been shown to have a pivotal role in the initiation and evolution of multiple tumors, but its function in hepatocellular carcinoma (HCC) requires further elucidation.
circUGP2 (hsa_circ_0001020) was identified in the GEO database by HCC circRNA microarray. Subsequently, an assessment was conducted to determine the biological effects of circUGP2, employing a series of analytical methods, including CCK8, EdU, colony formation, transwell, scratch assays, and in vivo experimentation. To explore the functions of circUGP2 as a sponge, including RNA pull-down, microRNA-seq, fluorescence in situ hybridization (FISH), RNA immunoprecipitation (RIP), and luciferase reporter assays were employed. Mass spectrometry (MS), RIP, and co-inmunoprecipitation (Co-IP) were employed to examine the interaction between cirrcUGP2 and up-frameshift protein 1 (UPF1).
circUGP2 was downregulated in HCC tissues and cells, which inhibited the growth and spread of HCC in vitro and in vivo. In the mechanisms, circUGP2 has the capacity to modulate KLF4 by sponging miR-137-3p, thereby suppressing HCC growth and migration. In addition, circUGP2 could combine with UPF1 and facilitate an interplay between UPF1 and AKT, influencing tumor progression in HCC via inactivation of the PI3K/AKT signaling pathway.
circUGP2 has a crucial function in HCC development by modulating the miR-137-3p/KLF4 axis to inactivate the PI3K/AKT/mTOR pathway and by interacting with UPF1. The findings indicate the potential of circUGP2 as a novel biomarker and target for HCC.

PMID:
42890918
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.

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