Evidence map›Paper›PMID 42734688›Full record

ArticleScience China. Life sciences2026

Mint3 suppresses cuproptosis by modulating the AHR signalling pathway to facilitate the progression of hepatocellular carcinoma.

Jianling Xia, Jialing Xiao, Zhilin Jiang, Chanyu Xiong, Yun Zhang, Feng Pu, Juanjuan Ji, Xiao Wang, Shikai Zhu, Bo Gong and 1 more

Abstract read
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Article in Science China. Life sciences, 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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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Jianling XiaGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Jialing XiaoGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Zhilin JiangGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Chanyu XiongGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yun ZhangGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Feng PuGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Juanjuan JiGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Xiao WangGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Shikai ZhuSichuan Provincial Key Laboratory for Clinical Immunology Translational Medicine, Organ Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Bo GongGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yu ZhouGenetic Diseases Key Laboratory of Sichuan Province, Medical Genetics and Rare Diseases Center, Department of Laboratory Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China. zhouyu422@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We screened genes from multiple datasets that were highly expressed in hepatocellular carcinoma (HCC) and associated with prognosis, and identified Mint3 as an important oncogene. Mint3 is implicated in controlling the malignant behaviours of pancreatic and breast cancer cells; however, our understanding of its role in HCC remains limited. Bioinformatic analysis of the underlying mechanisms showed that Mint3 may accelerate HCC development by suppressing cuproptosis. Cuproptosis, a novel copper-induced mode of cell death, may be associated with tumour progression. However, its involvement in tumourigenesis, metastasis, and patient prognosis requires further investigation. In this study, we aimed to identify novel biomarkers for HCC that may improve the prognosis of patients with HCC. We also investigated whether Mint3 regulated cuproptosis in HCC cells. Our results showed that Mint3 expression was frequently elevated in HCC specimens and was associated with increased tumour size, advanced tumour-node-metastasis stage, higher pathological grade, and poorer survival. Mint3 affected cell morphology and promoted proliferation, migration, and the epithelial-mesenchymal transition of HCC cells. Furthermore, our findings revealed that Mint3 overexpression resulted in reduced cuproptosis in HCC cells. The overexpression/down-regulation of FDX1, which is a critical mediator of cuproptosis, reversed Mint3 overexpression/downregulation-induced alterations of malignant phenotypes of HCC cells. Mechanistically, Mint3 exerted this effect via direct interaction with AHR, thus modulating the AHR signalling pathway and promoting AHR nuclear translocation. Further research demonstrated that AHR binds to the promoter region of FDX1 and subsequently inhibits it. Meanwhile, Mint3 knockdown suppressed HCC progression in patient-derived xenograft models. In the Mint3-knockout mouse group, Tp53 knockout/c-Myc overexpression treatment induced less spontaneous tumour formation than that in the WT group. Collectively, Mint3 is overexpressed in HCC and contributes to HCC progression by inhibiting cuproptosis via the AHR signalling pathway. Therefore, Mint3 may serve as a potential biomarker and therapeutic target in HCC.

Indexed as

AHRcuproptosisFDX1hepatocellular carcinomaMint3

Identifiers

PMID42734688

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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.