ArticleJournal of cellular physiology2008
Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating EGFR-dependent PI3K/Akt signaling.
Article in Journal of cellular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- The Impact of Cholecystectomy on Colorectal Cancer Risk: A Comprehensive Review on Risk Factors and the Association.Current gastroenterology reports · 2025Review
- The effects of metabolism on the immune microenvironment in colorectal cancer.Cell death discovery · 2024Review
- Hyodeoxycholic acid inhibits colorectal cancer proliferation through the FXR/EREG/EGFR axis.Frontiers in cell and developmental biology · 2024Article
- Muscarinic receptor agonist-induced βPix binding to β-catenin promotes colon neoplasia.Scientific reports · 2023Article
- CHRM3-Associated miRNAs May Play a Role in Bile Acid-Induced Proliferation of H508 Colon Cancer Cells.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- Relationships between gut microbiota, red meat consumption and colorectal cancer.Journal of carcinogenesis & mutagenesis · 2022Article
- Benign gallbladder disease is a risk factor for colorectal cancer, but cholecystectomy is not: A propensity score matching analysis.Frontiers in oncology · 2022Article
- Alterations in the Gut Microbiota and Their Metabolites in Colorectal Cancer: Recent Progress and Future Prospects.Frontiers in oncology · 2022Review
- Cholesterol Promotes Colorectal Cancer Growth by Activating the PI3K/AKT Pathway.Journal of oncology · 2022Article
- Lithocholic Acid Induces miR21, Promoting PTEN Inhibition via STAT3 and ERK-1/2 Signaling in Colorectal Cancer Cells.International journal of molecular sciences · 2021Article
- Colon Carcinogenesis: The Interplay Between Diet and Gut Microbiota.Frontiers in cellular and infection microbiology · 2020Review
- The Role of M3 Muscarinic Receptor Ligand-Induced Kinase Signaling in Colon Cancer Progression.Cancers · 2019Review
- Role of bile acids in colon carcinogenesis.World journal of clinical cases · 2018Review
- Targeting M3 Muscarinic Receptors for Colon Cancer Therapy.Current molecular pharmacology · 2018Review
- Interacting post-muscarinic receptor signaling pathways potentiate matrix metalloproteinase-1 expression and invasion of human colon cancer cells.The Biochemical journal · 2017Article
- HLBT-100: a highly potent anti-cancer flavanone fromCancer cell international · 2017Article
- Pathophysiological mechanisms of death resistance in colorectal carcinoma.World journal of gastroenterology · 2015Review
- Differential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancer.Digestive diseases and sciences · 2014Review
- Effect of a high-fat diet in development of colonic adenoma in an animal model.World journal of gastroenterology · 2014Article
- The role of FAK in tumor metabolism and therapy.Pharmacology & therapeutics · 2014Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Recent studies indicate that secondary bile acids promote colon cancer cell proliferation but their role in maintaining cell survival has not been explored. We found that deoxycholyltaurine (DCT) markedly attenuated both unstimulated and TNF-alpha-stimulated programmed cell death in colon cancer cells by a phosphatidylinositol 3-kinase (PI3K)-dependent mechanism. To examine the role of bile acids and PI3K signaling in maintaining colon cancer cell survival, we explored the role of signaling downstream of bile acid-induced activation of the epidermal growth factor receptor (EGFR) in regulating both apoptosis and proliferation of HT-29 and H508 human colon cancer cells. DCT caused dose- and time-dependent Akt (Ser(473)) phosphorylation, a commonly used marker of activated PI3K/Akt signaling. Both EGFR kinase and PI3K inhibitors attenuated DCT-induced Akt phosphorylation and Akt activation, as demonstrated by reduced phosphorylation of a GSK-3-paramyosin substrate. Transfection of HT-29 cells with kinase-dead EGFR (K721M) reduced DCT-induced Akt phosphorylation. In HT-29 cells, EGFR and PI3K inhibitors as well as transfection with dominant negative AKT attenuated DCT-induced cell proliferation. DCT-induced PI3K/Akt activation resulted in downstream phosphorylation of GSK-3 (Ser(21/9)) and BAD (Ser(136)), and nuclear translocation (activation) of NF-kappaB, thereby confirming that DCT-induced activation of PI3K/Akt signaling regulates both proproliferative and prosurvival signals. Collectively, these results indicate that DCT-induced activation of post-EGFR PI3K/Akt signaling stimulates both colon cancer cell survival and proliferation.
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Registered trials
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.