ArticleJournal of cellular and molecular medicine2020
Alpha-fetoprotein accelerates the progression of hepatocellular carcinoma by promoting Bcl-2 gene expression through an RA-RAR signalling pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Functional and Genetic Analyses Unveil the Implication ofJournal of developmental biology · 2026Article
- Alpha fetoprotein (AFP)-producing gastric cancer: clinicopathological features and treatment strategies.Cell & bioscience · 2025Review
- Exploring the Multifunctional Role of Alpha-Fetoprotein in Cancer Progression: Implications for Targeted Therapy in Hepatocellular Carcinoma and Beyond.International journal of molecular sciences · 2025Review
- Targeting AFP-RARβ complex formation: a potential strategy for treating AFP-positive hepatocellular carcinoma.Molecular diversity · 2025Article
- Prognostic analysis of different postoperative adjuvant therapies for patients with hepatocellular carcinoma after radical resection with high-risk recurrence factors: a multicenter real-world retrospective study.Frontiers in immunology · 2025Article
- Enhancing survival outcomes in unresectable hepatocellular carcinoma: a prospective cohort study on the effects of Huaier granules with targeted therapy plus immunotherapy.Frontiers in pharmacology · 2025Article
- Alpha-fetoprotein: Past, present, and future.Hepatology communications · 2024Review
- Diagnostic Efficacy and Possible Underlying Mechanisms of Noninvasive Clinical Markers in Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2023Article
- Structural requirement of RARγ agonism through computational aspects.Journal of molecular modeling · 2023Article
- A novel nomogram based on GD for predicting prognosis in hepatocellular carcinoma.Frontiers in oncology · 2023Article
- All-trans retinoic acid inhibits the malignant behaviors of hepatocarcinoma cells by regulating ferroptosis.Genes & diseases · 2022Article
- α-Fetoprotein fragment synergizes with sorafenib to inhibit hepatoma cell growth and migration and promote the apoptosis.Journal of cellular and molecular medicine · 2022Article
- Serum alpha-fetoprotein as a predictive biomarker for tissue alpha-fetoprotein status and prognosis in patients with hepatocellular carcinoma.Translational cancer research · 2022Article
- Retinoids in the Pathogenesis and Treatment of Liver Diseases.Nutrients · 2022Review
- Identification of Clinical Phenotypes and Related Survival in Patients with Large HCCs.Cancers · 2021Article
- AFP-Inhibiting Fragments for Drug Delivery: The Promise and Challenges of Targeting Therapeutics to Cancers.Frontiers in cell and developmental biology · 2021Review
- Alpha-Fetoprotein Binding Mucin and Scavenger Receptors: An Available Bio-Target for Treating Cancer.Frontiers in oncology · 2021Review
- Alpha-fetoprotein accelerates the progression of hepatocellular carcinoma by promoting Bcl-2 gene expression through an RA-RAR signalling pathway.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have found that alpha-fetoprotein (AFP) can promote the proliferation of hepatoma cells and accelerate the progression of hepatocellular carcinoma (HCC). However, the exact mechanism of action remains unclear. Recent bioinformatics studies have predicted the possible interaction between AFP and retinoic acid receptors (RARs). Thus, the purpose of this study was to investigate the molecular mechanism through which AFP promotes tumour cell proliferation by interfering with the RA-RAR signal pathway. Our data indicated that AFP could significantly promote the proliferation and weaken ATRA-induced apoptosis of hepatoma cells. Besides, cytoplasmic AFP interacts with RAR, disrupting its entrance into the nucleus, which in turn affects the expression of the Bcl-2 gene. In addition, knockdown of AFP in HepG2 cells was synchronously associated with an incremental increase of RAR binding to DNA, as well as down-regulation of Bcl-2; the opposite effect was observed in AFP gene-transfected HLE cells. Moreover, a similar effect of AFP was detected in tumour tissues with high serum AFP, but not in adjacent non-cancerous liver tissues, or HCC tissues with low serum AFP levels. These results indicate that AFP acts as signalling molecule and prevents RAR from entering into the nucleus by interacting with RAR, thereby promoting the expression of Bcl-2. Our data reveal a novel mechanism through which AFP regulates Bcl-2 expression and further suggest that AFP may be used as a novel target for treating HCC.
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