ArticleCell cycle (Georgetown, Tex.)2017
Oncogenic retinoic acid receptor γ knockdown reverses multi-drug resistance of human colorectal cancer via Wnt/β-catenin pathway.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 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
- New Fluorescent Synthetic Retinoids as Potential RAR Agonists with Anticancer, Molecular Docking and ADME Assessments.Journal of fluorescence · 2025Article
- The Emerging Oncogenic Role of RARγ: From Stem Cell Regulation to a Potential Cancer Therapy.International journal of molecular sciences · 2025Review
- ZSH-2208: A novel retinoid with potent anti-tumour effects on ESCC stem cells via RARγ-TNFAIP3 axis.Clinical and translational medicine · 2025Article
- Comprehensive review of the resistance mechanisms of colorectal cancer classified by therapy type.Frontiers in immunology · 2025Review
- Molecular Interactions of Selective Agonists and Antagonists with the Retinoic Acid Receptor γ.International journal of molecular sciences · 2024Review
- Alteration in the expression of the chemotherapy resistance‑related genes in response to chronic and acute hypoxia in pancreatic cancer.Biomedical reports · 2023Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Deregulation of All-International journal of molecular sciences · 2023Review
- Recent Advances in Transcription Factors Biomarkers and Targeted Therapies Focusing on Epithelial-Mesenchymal Transition.Cancers · 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
- Targeting the retinoic acid signaling pathway as a modern precision therapy against cancers.Frontiers in cell and developmental biology · 2023Review
- Dihydrotanshinone I Inhibits the Proliferation and Growth of Oxaliplatin-Resistant Human HCT116 Colorectal Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- Antagonizing RARγ Drives Necroptosis of Cancer Stem Cells.International journal of molecular sciences · 2022Review
- Lessons to cancer from studies of leukemia and hematopoiesis.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoic acid receptor γ (RARγ), a unique member of the nuclear receptor superfamily, plays an important role in the progression of several cancers such as hepatocellular carcinoma, esophageal cancer, and cholangiocarcinoma. However, little is known about the regulatory mechanism of the RARγ expression in colorectal cancer (CRC) progression. In the present study, we found that RARγ was frequently overexpressed in human CRC specimens and CRC cell lines, and it mainly resided in the cytoplasm in CRC specimens. Tissue microarrays showed that RARγ indicated vital clinical significance in CRC. RARγ knockdown neither affected CRC cell proliferation nor blocked the cell cycle of CRC cells. However, RARγ knockdown increased the sensitivity of CRC cells to chemotherapeutics through downregulation of multi-drug resistance 1(MDR1). Further studies suggested that RARγ knockdown resulted in downregulation of MDR1, in parallel with suppression of the Wnt/β-catenin pathway. Moreover, a significantly positive association between RARγ and MDR1 was demonstrated in CRC tissue microarrays. Collectively, these results suggested that overexpression of RARγ contributed to the multidrug chemoresistance of CRC cells, at least in part due to upregulation of MDR1 via activation of the Wnt/β-catenin pathway, indicating that RARγ might serve as a potential therapeutic target for chemoresistant CRC patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.