ArticleCancer science2021
GPR126 regulates colorectal cancer cell proliferation by mediating HDAC2 and GLI2 expression.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
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- Domain-specific N-glycosylation of the adhesion G-protein-coupled receptor ADGRG6 N-terminal fragment regulates trafficking, proteolytic processing, and signaling.Molecular biology of the cell · 2025Article
- Investigation of the cytotoxic effects and mechanisms of the SLC39A6-targeting ADC drug BRY812 in CRC.Scientific reports · 2025Article
- Nutritional ketosis modulates the methylation of cancer-related genes in patients with obesity and in breast cancer cells.Journal of physiology and biochemistry · 2025Article
- Mechanosensitive adhesion G protein-coupled receptors: Insights from health and disease.Genes & diseases · 2025Review
- Identification of a novel prognostic marker ADGRG6 in pancreatic adenocarcinoma: multi-omics analysis and experimental validation.Frontiers in immunology · 2025Article
- Molecular characteristics and cancer immunity of LRP1B and its relationship with the Hedgehog signaling pathway in colorectal cancer.Frontiers in immunology · 2025Article
- Machine Learning Developed a MYC Expression Feature-Based Signature for Predicting Prognosis and Chemoresistance in Pancreatic Adenocarcinoma.Biochemical genetics · 2024Article
- Inhibition of ADAM9 promotes the selective degradation of KRAS and sensitizes pancreatic cancers to chemotherapy.Nature cancer · 2024Article
- SOX4/HDAC2 Axis Enhances Cell Survivability and Reduces Apoptosis by Activating AKT/MAPK Signaling in Colorectal Cancer.Digestive diseases and sciences · 2024Article
- Structure, ligands, and roles of GPR126/ADGRG6 in the development and diseases.Genes & diseases · 2024Review
- The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability.Cell reports · 2023Article
- Detection of the ADGRG6 hotspot mutations in urine for bladder cancer early screening by ARMS-qPCR.Cancer medicine · 2023Article
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- A novel variant in NBAS identified from an infant with fever-triggered recurrent acute liver failure disrupts the function of the gene.Human genome variation · 2023Article
- HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023Review
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Progesterone activates GPR126 to promote breast cancer development via the Gi pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The G-protein-coupled receptor 126 (GPR126) may play an important role in tumor development, although its role remains poorly understood. We found that GPR126 had higher expression in most colorectal cancer cell lines than in normal colon epithelial cell lines, and higher expression levels in colorectal cancer tissues than in normal adjacent colon tissues. GPR126 knockdown induced by shRNA inhibited cell viability and colony formation in HT-29, HCT116, and LoVo cells, decreased BrdU incorporation into newly synthesized proliferating HT-29 cells, led to an arrest of cell cycle progression at the G1 phase in HCT-116 and HT-29 cells, and suppressed tumorigenesis of HT-29, HCT116, and LoVo cells in nude mouse xenograft models. GPR126 knockdown engendered decreased transcription and translation of histone deacetylase 2 (HDAC2), previously implicated in the activation of GLI1 and GLI2 in the Hedgehog signaling pathway. Ectopic expression of HDAC2 in GPR126-silenced cells restored cell viability and proliferation, GLI2 luciferase reporter activity, partially recovered GLI2 expression, and reduced the cell cycle arrest. HDAC2 regulated GLI2 expression and, along with GLI2, it bound to the PTCH1 promoter, as evidenced by a chip assay with HT-29 cells. Purmorphamine, a hedgehog agonist, largely restored the cell viability and expression of GLI2 proteins in GPR126-silenced HT-29 cells, whereas GANT61, a hedgehog inhibitor, further enhanced the GPR126 knockdown-induced inhibitory effects. Our findings demonstrate that GPR126 regulates colorectal cancer cell proliferation by mediating the expression of HDAC2 and GLI2, therefore it may represent a suitable therapeutic target for colorectal cancer treatment.
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