ArticleMolecular and cellular biology2013
Oncogenic activity of retinoic acid receptor γ is exhibited through activation of the Akt/NF-κB and Wnt/β-catenin pathways in cholangiocarcinoma.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 61 citations in OpenAlex.
- Retinoic Acid Receptor γ Is a Ligand-Activated Gatekeeper to Stem Cell Developmental Progression.International journal of molecular sciences · 2026Review
- Retinoic Acid Receptor γ Activity Plays a Critical Role in Regulating Early Mouse Gastruloid Development.International journal of molecular sciences · 2026Article
- The role of RARG in solid tumor progression and therapeutic potential.Discover oncology · 2026Review
- The Influences of RARγ on the Behavior of Normal and Cancer Stem Cells.International journal of molecular sciences · 2026Review
- The Emerging Oncogenic Role of RARγ: From Stem Cell Regulation to a Potential Cancer Therapy.International journal of molecular sciences · 2025Review
- Hepatic Nuclear Receptors in Cholestasis-to-Cholangiocarcinoma Pathology.The American journal of pathology · 2025Review
- ZSH-2208: A novel retinoid with potent anti-tumour effects on ESCC stem cells via RARγ-TNFAIP3 axis.Clinical and translational medicine · 2025Article
- Oncogenic RARγ isoforms promote head and neck cancer proliferation through vinexin-β-mediated cell cycle acceleration and autocrine activation of EGFR signal.International journal of biological sciences · 2025Article
- Unveiling the role of RARs in stomach adenocarcinoma: clinical implications and prognostic biomarkers.Translational cancer research · 2024Article
- Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.International journal of molecular sciences · 2024Review
- Oligandrin fromHeliyon · 2024Article
- Deregulation of All-International journal of molecular sciences · 2023Review
- Blockage of retinoic acid signaling via RARγ suppressed the proliferation of pancreatic cancer cells by arresting the cell cycle progression of the G1-S phase.Cancer cell international · 2023Article
- Targeting the Retinoic Acid Pathway to Eradicate Cancer Stem Cells.International journal of molecular sciences · 2023Review
- Retinoic acid receptor regulation of decision-making for cell differentiation.Frontiers in cell and developmental biology · 2023Review
- Antagonizing RARγ Drives Necroptosis of Cancer Stem Cells.International journal of molecular sciences · 2022Review
- High expression of RARG accelerates ovarian cancer progression by regulating cell proliferation.Frontiers in oncology · 2022Article
- Lessons to cancer from studies of leukemia and hematopoiesis.Frontiers in cell and developmental biology · 2022Review
- Integrative chemogenomic analysis identifies small molecules that partially rescue ΔF508-CFTR for cystic fibrosis.CPT: pharmacometrics & systems pharmacology · 2021Article
- The RARγ Oncogene: An Achilles Heel for Some Cancers.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant expression and function of retinoic acid receptor γ (RARγ) are often involved in the progression of several cancers. However, the role of RARγ in cholangiocarcinoma (CCA), chemoresistant bile duct carcinoma with a poor prognosis, remains unclear. In the present study, we found that RARγ was frequently overexpressed in human CCA specimens. Its overexpression was associated with poor differentiation, lymph node metastasis, high serum carbohydrate antigen 19-9 level, and poor prognosis of CCA. Downregulation of RARγ reduced CCA cell proliferation, migration, invasion, and colony formation ability in vitro and tumorigenic potential in nude mice. RARγ knockdown resulted in upregulation of cell cycle inhibitor P21, as well as downregulation of cyclin D1, proliferating cell nuclear antigen, and matrix metallopeptidase 9, in parallel with suppression of the Akt/NF-κB pathway. Furthermore, overexpression of RARγ contributed to the multidrug chemoresistance of CCA cells, at least in part due to upregulation of P glycoprotein via activation of the Wnt/β-catenin pathway. Molecular mechanism studies revealed that RARγ interacted with β-catenin and led to β-catenin nuclear translocation. Taken together, our results suggested that RARγ plays an important role in the proliferation, metastasis, and chemoresistance of CCA through simultaneous activation of the Akt/NF-κB and Wnt/β-catenin pathways, serving as a potential molecular target for CCA treatment.
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