ArticleScientific reports2025
HOPX regulates the invasion and migration abilities of hepatocellular carcinoma by targeting SNAIL.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Metformin suppressed epithelial-mesenchymal transition, cisplatin resistance and metastatic potential of ovarian cancer via inhibiting TGF-β1/Smads.Translational cancer research · 2026Article
- Molecular classification and construction of prognostic risk model via machine learning based on metabolic-related genes in hepatocellular carcinoma.Translational cancer research · 2026Article
- Review
- Shared and Context-Specific Mechanisms of EMT and Cellular Plasticity in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
HOPX acts as a tumor suppressor in certain cancers, but the function of HOPX, as well as its mechanism of action in hepatocellular carcinoma (HCC) has not been fully elucidated. In this study, using in vitro and in vivo animal models, the effect of HOPX on the development of HCC was explored. In our study, the HOPX expression at both protein and mRNA level were found to be downregulated in HCC cells and tumor tissues. Restoration of HOPX expression was found to inhibit HCC cell invasion and migration capabilities, but produced no effect on growth. Moreover, HOPX prevented metastasis in an HCC cell metastatic mouse model. Further investigations showed that HOPX could suppress HCC cell epithelial-to-mesenchymal transition (EMT) by inhibiting SNAIL, an EMT transcription factor that is required for the metastasis-inhibition activity of HOPX to proceed. Our study identified HOPX as a suppressor of the development of HCC, which implies that HOPX suppresses HCC cells invasion and migration by inhibiting SNAIL.
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