ArticleMolecular and cellular biochemistry2023
Folic acid depletion along with inhibition of the PERK arm of endoplasmic reticulum stress pathway promotes a less aggressive phenotype of hepatocellular carcinoma cells.
Article in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- Inhibition of PERK signaling suppresses tumor progression and blocks GP73-GRP78-dependent stromal activation in hepatocellular carcinoma.Neoplasia (New York, N.Y.) · 2026Article
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Translational issues with phototherapy of cancer.Translational oncology · 2026Review
- Molecular classification and construction of prognostic risk model via machine learning based on metabolic-related genes in hepatocellular carcinoma.Translational cancer research · 2026Article
- PERK/ATF4/LAMP3-arm contributes to the aggressive phenotype of hepatocellular carcinoma cells in response to the chronic ethanol exposure.Scientific reports · 2026Article
- Targeting the unfolded protein response in cancer: mechanisms, small-molecule inhibitors, and translational challenges.Frontiers in immunology · 2026Review
- FUT3 mediated GRP78 fucosylation promotes colorectal cancer survival and proliferation under glucose restriction via PERK/ATF4/STC2 axis.NPJ precision oncology · 2025Article
- Large scale plasma proteomic profiles improve prediction of idiopathic pulmonary fibrosis in general population.Respiratory research · 2025Article
- Balancing the scales: folic acid and vitamin B12 in the aggressiveness of hepatocellular carcinoma.Clinical and experimental medicine · 2025Article
- Article
- Deciphering the nexus between long non-coding RNAs and endoplasmic reticulum stress in hepatocellular carcinoma: biomarker discovery and therapeutic horizons.Cell death discovery · 2024Review
- GSK2606414 Sensitizes ABCG2-Overexpressing Multidrug-Resistant Colorectal Cancer Cells to Chemotherapeutic Drugs.Biomedicines · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Folate is a vital vitamin involved in one-carbon metabolism and any changes in folate status may lead to epigenetic alterations. It is already known that stages and liver cancer progression are negatively correlated with folate levels. Nevertheless, mechanisms involved in folate deficiency in HCC (Hepatocellular carcinoma) are still not completely understood. So, this study tests the hypothesis that due to the increased demand for ER (endoplasmic reticulum) proteins, folate deficiency might lead to the induction of UPR (unfolded protein response), which is further correlated with HCC outcomes. HCC cells were cultured in both folate normal (FN) and folate deficient (FD) conditions and the expression of genes of ER stress pathway was investigated. The results demonstrated activation of UPR via induction of PERK, ATF4, and LAMP3. Besides this, FD reduced the migratory capacity and the invasiveness of HCC cells along with the reduction in mesenchymal markers like vimentin but increased apoptosis. Treatment with GSK2606414 (PERK inhibitor) decreased the FD induced expression of PERK, ATF4, and LAMP3 in FD cells. Also, GSK2606414 was found to increase apoptotic cell death and to further reduce the cancer hallmarks selectively in FD cells but not in FN cells. Altogether, our data suggest that targeting the ER stress pathway along with folate deficiency may provide a more promising elimination of the metastatic potential of HCC cells contributing to more effective therapeutic agents.
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