ArticleJournal of translational medicine2013
Insufficient radiofrequency ablation promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells through Akt and ERK signaling pathways.
Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 81 citations in OpenAlex.
- Percutaneous laser ablation: a new contribution to unresectable high-risk metastatic retroperitoneal lesions?Oncotarget · 2017Trial
- Residual Lung Cancer After Incomplete Microwave Ablation Exhibits cGAS-STING-ZEB1-Driven Malignant Progression.Cancers · 2026Article
- Biomaterial-based strategies for postoperative residual tumors: From margin clearance to immune control and tissue repair.Materials today. Bio · 2026Review
- Sublethal heat stress synergizes with the tumor microenvironment to drive recurrence of hepatocellular carcinoma after thermal ablation: mechanisms, molecular predictors, and targeted interventions.Cell biology and toxicology · 2026Review
- Verteporfin-loaded hydrogel targeting YAP-mediated MDSCs recruitment for the treatment of residual tumors after incomplete radiofrequency ablation.Theranostics · 2026Article
- Research Progress on the Molecular Mechanism of Metformin Regulating AMPK Signaling Pathway in Inhibiting Liver Cancer.OncoTargets and therapy · 2026Review
- Structural Control for Tunable Hyperthermia-Induced Cellular Responses Using 3D-Printed Platforms.ACS biomaterials science & engineering · 2025Article
- Ruthenium Complex Suppresses Proliferation of Residual Hepatocellular Carcinoma after Incomplete Radiofrequency Ablation Therapy.Recent patents on anti-cancer drug discovery · 2025Article
- Mechanisms of rapid tumor progression after insufficient radiofrequency ablation of hepatocellular carcinoma.Frontiers in cell and developmental biology · 2025Review
- ATPase Inhibitory Factor 1 Drives Mitochondrial Energy Metabolic Reprogramming to Promote HCC Vasculogenic Mimicry via the ESR1/miR-20a-3p/GNAZ Pathway.Research (Washington, D.C.) · 2025Article
- SAR1A Induces Cell Growth and Epithelial-Mesenchymal Transition Through the PI3K/AKT/mTOR Pathway in Head and Neck Squamous Cell Carcinoma: An In Vitro and In Vivo Study.Biomedicines · 2024Article
- Review
- Article
- Melatonin enhances the efficacy of anti-PD-L1 by improving hypoxia in residual tumors after insufficient radiofrequency ablation.Journal of pharmaceutical analysis · 2024Article
- Clinical outcomes and tumor microenvironment response to radiofrequency ablation therapy: a systematic review and meta-analysis.Gland surgery · 2024Article
- Mechanisms and therapeutic strategies to combat the recurrence and progression of hepatocellular carcinoma after thermal ablation.Journal of interventional medicine · 2023Article
- Heat treatment-induced autophagy promotes breast cancer cell invasion and metastasis via TGF-PeerJ · 2023Article
- An Overview of Hepatocellular Carcinoma After Insufficient Radiofrequency Ablation.Journal of hepatocellular carcinoma · 2022Review
- Curcumin Prevents Epithelial-to Mesenchymal Transition-Mediated Ovarian Cancer Progression through NRF2/ETBR/ET-1 Axis and Preserves Mitochondria Biogenesis in Kidney after Cisplatin Administration.Advanced pharmaceutical bulletin · 2022Article
- Progression of hepatocellular carcinoma after radiofrequency ablation: Current status of research.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundResidual tumor progression after insufficient radiofrequency ablation (RFA) has been recently reported. However, whether epithelial-mesenchymal transition (EMT), which is a key process that drives cancer metastasis, is involved in the tumor progression after insufficient RFA is not well understood.
methodsHuman hepatocellular carcinoma (HCC) cell lines SMMC7721 and Huh7 were used. Insufficient RFA was simulated using a water bath (47°C 5 min, 10 min, 15 min, 20 min and 25 min gradually). MTT assay was used to evaluate the proliferation of HCC cells in vitro. Migration and invasion of HCC cells were determined by transwell assay. The molecular changes in HCC cells after insufficient RFA were evaluated by western blot. LY294002 and PD98059 were used to treat HCC cells. An ectopic nude mice model and a tail vein metastatic assay were used to evaluate the growth and metastatic potential of SMMC7721 cells in vivo after insufficient RFA.
resultsSMMC7721 and Huh7 cells after insufficient RFA (named as SMMC7721-H and Huh7-H respectively) exhibited enhanced proliferation, migration and invasion (6.4% and 23.6%, 33.2% and 66.1%, and 44.1% and 57.4% increase respectively) in vitro. Molecular changes of EMT were observed in SMMC7721-H and Huh7-H cells. LY294002 and PD98059 inhibited the EMT of SMMC7721-H and Huh7-H cells. SMMC7721-H cells also exhibited larger tumor size (1440.8±250.3 mm3 versus 1048.56±227.6 mm3) and more lung metastasis (97.4% increase) than SMMC7721 cells in vivo. Higher expression of PCNA, N-cadherin and MMP-2 and MMP-9, was also observed in SMMC7721-H tumors.
conclusionsInsufficient RFA could directly promote the invasiveness and metastasis of HCC cells. Insufficient RFA may promote the EMT of HCC cells through Akt and ERK signaling pathways.
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