ArticleNeoplasia (New York, N.Y.)2006
Increases in c-Src expression level and activity do not promote the growth of human colorectal carcinoma cells in vitro and in vivo.
Article in Neoplasia (New York, N.Y.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Article
- v-Src-driven transformation is due to chromosome abnormalities but not Src-mediated growth signaling.Scientific reports · 2018Article
- Cytokinesis Failure Leading to Chromosome Instability in v-Src-Induced Oncogenesis.International journal of molecular sciences · 2017Review
- v-Src Causes Chromosome Bridges in a Caffeine-Sensitive Manner by Generating DNA Damage.International journal of molecular sciences · 2016Article
- The blood-testis barrier and its implications for male contraception.Pharmacological reviews · 2012Review
- Src family kinase inhibitor Saracatinib (AZD0530) impairs oxaliplatin uptake in colorectal cancer cells and blocks organic cation transporters.Cancer research · 2010Article
- TRE17/USP6 oncogene translocated in aneurysmal bone cyst induces matrix metalloproteinase production via activation of NF-kappaB.Oncogene · 2010Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
- Protein kinase C delta is phosphorylated on five novel Ser/Thr sites following inducible overexpression in human colorectal cancer cells.Protein science : a publication of the Protein Society · 2007Article
- Increases in c-Yes expression level and activity promote motility but not proliferation of human colorectal carcinoma cells.Neoplasia (New York, N.Y.) · 2007Article
- Comparison of doxycycline delivery methods for Tet-inducible gene expression in a subcutaneous xenograft model.Journal of biomolecular techniques : JBT · 2007Article
- Tetracycline regulated systems in functional oncogenomics.Translational oncogenomics · 2007Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The levels and activity of c-Src in colorectal cancer cells increase steadily during the course of colorectal carcinogenesis and are most highly elevated in advanced metastatic disease. However, the effects of increases in c-Src activity on the proliferation of colorectal cancer cells during early and late stages of tumorigenesis remain elusive. To study the consequences of increases in c-Src levels and activity on the growth of colorectal cancer cells in later stages of colorectal carcinogenesis, we developed human colorectal cancer cell lines in which c-Src levels and activity could be inducibly increased by a tightly controlled expression of wild-type c-Src or of the constitutively active mutant of c-Src, c-SrcY527F. Src induction activated multiple signaling pathways (often associated with a proliferative response) but promoted neither cell proliferation in vitro nor tumor growth in a xenograft model in vivo. These results indicate that, in more advanced stages of colorectal carcinogenesis, increases in c-Src levels and activity are likely to have functions other than the direct promotion of tumor growth.
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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.