ArticleMolecular and cellular biology2009
Cross talk between receptor guanylyl cyclase C and c-src tyrosine kinase regulates colon cancer cell cytostasis.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Guanylate cyclase-C Signaling Axis as a theragnostic target in colorectal cancer: a systematic review of literature.Frontiers in oncology · 2023Pooled it
- Gut reactions and gut instincts: regulation of intestinal homeostasis by receptor guanylyl cyclase C (GC-C).The Biochemical journal · 2025Review
- Receptor Guanylyl Cyclase C and Cyclic GMP in Health and Disease: Perspectives and Therapeutic Opportunities.Frontiers in endocrinology · 2022Review
- The pseudokinase domain in receptor guanylyl cyclases.Methods in enzymology · 2022Review
- Sphingomyelin nanosystems loaded with uroguanylin and etoposide for treating metastatic colorectal cancer.Scientific reports · 2021Article
- Src regulates amino acid-mediated mTORC1 activation by disrupting GATOR1-Rag GTPase interaction.Nature communications · 2018Article
- The Guanylate Cyclase C-cGMP Signaling Axis Opposes Intestinal Epithelial Injury and Neoplasia.Frontiers in oncology · 2018Review
- SH2 Ligand-Like Effects of Second Cytosolic Domain of Na/K-ATPase α1 Subunit on Src Kinase.PloS one · 2015Article
- Intestinal cell proliferation and senescence are regulated by receptor guanylyl cyclase C and p21.The Journal of biological chemistry · 2014Article
- SRC-family tyrosine kinases in oogenesis, oocyte maturation and fertilization: an evolutionary perspective.Advances in experimental medicine and biology · 2014Review
- Site-specific N-linked glycosylation of receptor guanylyl cyclase C regulates ligand binding, ligand-mediated activation and interaction with vesicular integral membrane protein 36, VIP36.The Journal of biological chemistry · 2013Article
- Guanylate cyclase C deficiency causes severe inflammation in a murine model of spontaneous colitis.PloS one · 2013Article
- Crossing paths in Human Renal Cell Carcinoma (hRCC).International journal of molecular sciences · 2012Review
- Loss of guanylyl cyclase C (GCC) signaling leads to dysfunctional intestinal barrier.PloS one · 2011Article
- Defying the stereotype: non-canonical roles of the Peptide hormones guanylin and uroguanylin.Frontiers in endocrinology · 2011Article
- Receptor guanylyl cyclase C (GC-C): regulation and signal transduction.Molecular and cellular biochemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased activation of c-src seen in colorectal cancer is an indicator of a poor clinical prognosis, suggesting that identification of downstream effectors of c-src may lead to new avenues of therapy. Guanylyl cyclase C (GC-C) is a receptor for the gastrointestinal hormones guanylin and uroguanylin and the bacterial heat-stable enterotoxin. Though activation of GC-C by its ligands elevates intracellular cyclic GMP (cGMP) levels and inhibits cell proliferation, its persistent expression in colorectal carcinomas and occult metastases makes it a marker for malignancy. We show here that GC-C is a substrate for inhibitory phosphorylation by c-src, resulting in reduced ligand-mediated cGMP production. Consequently, active c-src in colonic cells can overcome GC-C-mediated control of the cell cycle. Furthermore, docking of the c-src SH2 domain to phosphorylated GC-C results in colocalization and further activation of c-src. We therefore propose a novel feed-forward mechanism of activation of c-src that is induced by cross talk between a receptor GC and a tyrosine kinase. Our findings have important implications in understanding the molecular mechanisms involved in the progression and treatment of colorectal cancer.
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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.