ArticleCell biochemistry and biophysics2025
MICAL1 Mediates TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Metastasis of Hepatocellular Carcinoma by Activating Smad2/3.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Exosomal circ-ZNF652 Mediates TGF-β1-Induced Epithelial-Mesenchymal Transition and Glycolytic Reprogramming to Promote Hepatocellular Carcinoma Progression.Journal of microbiology and biotechnology · 2026Article
- MMT: A Potential Mechanism of Myocardial Fibrosis - Regulation of the TGF-β1/Smad3 Pathway and Prospects for Targeted Therapy.Reviews in cardiovascular medicine · 2026Review
- MICAL1 Contributes to Myogenic Differentiation by Modulating Actin Remodeling and YAP1 Nuclear Localization in C2C12 Myoblasts.International journal of molecular sciences · 2026Article
- TGF-β in tumor development and progression: mechanisms and therapeutics.Molecular biomedicine · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β (TGF-β) is involved in hepatocellular carcinoma (HCC) growth and metastasis. Our study aimed to investigate the role of molecules interacting with CasL 1 (MICAL1) in regulating TGF-β-triggered EMT in HCC and the related mechanisms. After detecting MICAL1 expression and prognostic value in HCC, in vitro assays including CCK-8 assay, EdU staining, flow cytometry assay, Transwell assay, western blotting, and RT-qPCR and in vivo metastasis assay was conducted to evaluate the influence of MICAL1 knockdown on the proliferation and apoptosis as well as TGF-β-induced EMT and metastasis of Huh7 and MHCC97H cells. MICAL1 was highly expressed in HCC, and its high expression was related to histological grade, TNM stage, and shorter overall survival of HCC patients. MICAL1 silencing suppressed proliferation, promoted apoptosis, and curbed TGF-β1-triggered cytoskeletal remodeling, EMT, and metastasis of HCC cells. MICAL1 knockdown impeded TGF-β1-induced upregulation in phosphorylated-Smad2/3 protein levels and reduced Smad2/3 mRNA levels in HCC cells. MICAL1 downregulation enhanced the polyubiquitination and proteasomal degradation of TβRI. Additionally, MICAL1 silencing suppressed tumor growth and lung metastasis in Huh7-derived xenograft mouse models. Collectively, MICAL1 knockdown impairs TGF-β1-stimulated EMT and metastasis of HCC cells by restraining Smad2/3 phosphorylation and activation.
Indexed as
Identifiers
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Registered trials
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.