ArticleAmerican journal of cancer research2024
Inactivation of ERK1/2 in cancer-associated hepatic stellate cells suppresses cancer-stromal interaction by regulating extracellular matrix in fibrosis.
Article in American journal of cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Targeted Therapy and Immunotherapies in Hepatocellular Carcinoma: Mechanisms and Clinical Studies.MedComm · 2026Review
- Hedyotis diffusa Willd suppresses hepatocellular carcinoma tumor-stromal interactions by inactivating cancer-associated hepatic stellate cells.Journal of gastrointestinal oncology · 2026Article
- Bibliometric analysis of MXRA7 gene research trajectory: trends and insights (2015-2024).Discover oncology · 2025Article
- CCN5-Derived Peptide Ameliorates Liver Fibrosis in Mice through Inhibiting the ERK1/2 and PI3K Signaling Pathways.ACS omega · 2025Article
- Multiorgan crosstalk in MASLD/MASH: from hepatic pathogenesis to systemic complications.Frontiers in endocrinology · 2025Review
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
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Abstract
The ERK1/2 pathway is involved in epithelial-mesenchymal transformation and cell cycle of tumor cells in hepatocellular carcinoma (HCC). In the present study, we investigated the involvement of ERK1/2 activation on hepatic stellate cells (HSCs). We identified ERK1/2 phosphorylation in activated HSCs of HCC samples. We found that tumor cells promoted the migration and invasion capacity of HSCs by activating ERK1/2 phosphorylation. Using high throughput transcriptome sequencing analysis, we found that ERK1/2 inhibition altered genes significantly correlated to signaling pathways involved in extracellular matrix remodeling. We screened genes and demonstrated that the ERK1/2 inhibition-related gene set significantly correlated to cancer-associated fibroblast infiltration in TCGA HCC tumor samples. Moreover, inhibition of ERK1/2 suppressed tumor cell-induced enhancement of HSC migration and invasion by regulating expression of fibrosis markers FAP, FN1 and COL1A1. In a tumor cell and HSC splenic co-transplanted xenograft mouse model, inhibition of ERK1/2 suppressed liver tumor formation by downregulating fibrosis, indicating ERK1/2 inhibition suppresses tumor-stromal interactions
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