ArticleInternational journal of oncology2017
Sorafenib induces variations of the DNA methylome in HA22T/VGH human hepatocellular carcinoma-derived cells.
Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- External radiotherapy combined with sorafenib has better efficacy in unresectable hepatocellular carcinoma: a systematic review and meta-analysis.Clinical and experimental medicine · 2023Pooled it
- TET2 orchestrates YAP signaling to potentiate targetable vulnerability in hepatocellular carcinoma.Cell death & disease · 2025Article
- Mechanisms of drug resistance in hepatocellular carcinoma.Biological procedures online · 2025Review
- Comprehensive review and updated analysis of DNA methylation in hepatocellular carcinoma: From basic research to clinical application.Clinical and translational medicine · 2024Review
- TFCP2L1 drives stemness and enhances their resistance to Sorafenib treatment by modulating the NANOG/STAT3 pathway in hepatocellular carcinoma.Oncogenesis · 2024Article
- Evaluation of DNA methylation levels ofOncology reports · 2024Article
- NR0B1 augments sorafenib resistance in hepatocellular carcinoma through promoting autophagy and inhibiting apoptosis.Cancer science · 2024Article
- Roles and Mechanisms of Ferroptosis in Sorafenib Resistance for Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Review
- The Roles of Epigenetic Regulation and the Tumor Microenvironment in the Mechanism of Resistance to Systemic Therapy in Hepatocellular Carcinoma.International journal of molecular sciences · 2023Review
- Expression of Cellular and ExtracellularInternational journal of molecular sciences · 2022Article
- Long non-coding RNA ACTA2-AS1 inhibits the cisplatin resistance of non-small cell lung cancer cells through inhibiting autophagy by suppressing TSC2.Cell cycle (Georgetown, Tex.) · 2022Article
- Integrated Bioinformatic Analysis IdentifiesDisease markers · 2022Article
- Epigenome-wide association studies: current knowledge, strategies and recommendations.Clinical epigenetics · 2021Review
- Longitudinal Circulating Levels of miR-23b-3p, miR-126-3p and lncRNA GAS5 in HCC Patients Treated with Sorafenib.Biomedicines · 2021Article
- DNA methylation variations in familial female and male breast cancer.Oncology letters · 2021Article
- Epigenetic Regulation of Hepatocellular Carcinoma Progression through the mTOR Signaling Pathway.Canadian journal of gastroenterology & hepatology · 2021Review
- The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects.Signal transduction and targeted therapy · 2020Review
- Sorafenib- Taurine Combination Model for Hepatocellular Carcinoma Cells: Immunological Aspects.Asian Pacific journal of cancer prevention : APJCP · 2019Article
- Differential expression profiling of long non-coding RNA GAS5 and miR-126-3p in human cancer cells in response to sorafenib.Scientific reports · 2019Article
- HSP70 inhibitor VER155008 suppresses pheochromocytoma cell and xenograft growth by inhibition of PI3K/AKT/mTOR and MEK/ERK pathways.International journal of clinical and experimental pathology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sorafenib is currently used to treat advanced and/or unresectable hepatocellular carcinoma (HCC), but the increase of the median survival was only 3 months. Moreover, sorafenib has severe side effects and patients develop resistance quickly. Epigenetic alterations such as DNA methylation play a decisive role in the development and progression of HCC. To our knowledge, there are no studies that analysed the global DNA methylation changes in HCC cells treated with sorafenib. Using MeDip-chip technologies, we found 1230 differentially methylated genes in HA22T/VGH cells treated with sorafenib compared to untreated cells. Gene ontology and pathway analysis allowed identifying several enriched signaling pathways involved in tumorigenesis and cancer progression. Among the genes differentially methylated we found genes related to apoptosis, angiogenesis and invasion, and genes belonging to pathways known to be deregulated in HCC such as RAF/MEK/ERK, JAK-STAT, PI3K/AKT/mTOR and NF-κB. Generally, we found that oncogenes tended to be hypermethylated and the tumor suppressor genes tended to be hypomethylated after sorafenib treatment. Finally, we validated MeDip-chip results for several genes found differentially methylated such as BIRC3, FOXO3, MAPK3, SMAD2 and TSC2, using both COBRA assay and direct bisulfite sequencing and we evaluated their mRNA expression. Our findings suggest that sorafenib could affect the methylation level of genes associated to cancer-related processes and pathways in HCC cells, some of which have been previously described to be directly targeted by sorafenib.
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