USP37 facilitates hepatocellular carcinoma progression by deubiquitinating RAF1 and activating ERK1/2 signaling.

Yuming Wang, Ruidong Ding, Yilin Wang, Xiangheng Cai, Jijun Shan

Abstract read

In one paragraph

Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yuming WangInstitute of Organ Donation and Transplantation, Medical College of Qingdao University, Qingdao, 266000, China.

Ruidong DingInstitute of Organ Donation and Transplantation, Medical College of Qingdao University, Qingdao, 266000, China.

Yilin WangInstitute of Organ Donation and Transplantation, Medical College of Qingdao University, Qingdao, 266000, China.

Xiangheng CaiInstitute of Organ Donation and Transplantation, Medical College of Qingdao University, Qingdao, 266000, China. 17853736612@163.com.

Jijun ShanShanghai Medical College, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China. 1293996009@qq.com.

Funding

National Natural Science Foundation of China 82500972

6 · The paper itself

Abstract

USP37 plays a pivotal role in cell cycle regulation, oncogenesis and metastasis. So far, the precise mechanisms and function of USP37 in hepatocellular carcinoma (HCC) remain unclear. In this study, we found USP37 expression was significantly elevated in HCC tissues compared to adjacent normal tissues and high expression was negatively correlated with patient prognosis. Functional assays including CCK-8, EdU staining, colony formation assays, patient derived organoids, transwell assays, wound healing, and in vivo models demonstrated that USP37 significantly promoted proliferation and migration of HCC cells. Mechanistically, USP37 interacted with RAF1, enhancing its protein stability and activating the ERK signaling pathway. This study identifies a novel mechanism by which USP37 promotes HCC cell proliferation through stabilizing RAF1 and activating the RAF-ERK signaling pathway. These findings highlight USP37 as a potential therapeutic target for HCC.

Indexed as

Carcinoma, HepatocellularEndopeptidasesLiver NeoplasmsMAP Kinase Signaling SystemProto-Oncogene Proteins c-rafAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceUbiquitinationEndopeptidasesProto-Oncogene Proteins c-rafRaf1 protein, humanUSP37 protein, humanHepatocellular carcinomaRAF- ERK signaling pathwayUbiquitinationUSP37

Identifiers

PMID42337222

DOI10.1007/s10142-026-01931-y

What OpenQuestion holds

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Read underepoch 390

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None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.