ArticleOncogene2001
The mechanism of cell cycle regulation by v-Src.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 63 citations in OpenAlex.
- CircHAS2 activates CCNE2 to promote cell proliferation and sensitizes the response of colorectal cancer to anlotinib.Molecular cancer · 2024Article
- Anti-colorectal cancer of Ardisia gigantifolia Stapf. and targets prediction via network pharmacology and molecular docking study.BMC complementary medicine and therapies · 2023Article
- A Model for the Signal Initiation Complex Between Arrestin-3 and the Src Family Kinase Fgr.Journal of molecular biology · 2022Article
- EPS8 phosphorylation by Src modulates its oncogenic functions.British journal of cancer · 2020Article
- Blockade of HMGB1 signaling pathway by ethyl pyruvate inhibits tumor growth in diffuse large B-cell lymphoma.Cell death & disease · 2019Article
- Increased PTPRA expression leads to poor prognosis through c-Src activation and G1 phase progression in squamous cell lung cancer.International journal of oncology · 2017Article
- v-Src Causes Chromosome Bridges in a Caffeine-Sensitive Manner by Generating DNA Damage.International journal of molecular sciences · 2016Article
- Enhanced CaJournal of nanomaterials · 2013Article
- Dasatinib inhibits primary melanoma cell proliferation through morphology-dependent disruption of Src-ERK signaling.Oncology letters · 2013Article
- Identification of a Src tyrosine kinase/SIAH2 E3 ubiquitin ligase pathway that regulates C/EBPδ expression and contributes to transformation of breast tumor cells.Molecular and cellular biology · 2012Article
- c-Src inactivation reduces renal epithelial cell-matrix adhesion, proliferation, and cyst formation.American journal of physiology. Cell physiology · 2011Article
- Targeting SRC in glioblastoma tumors and brain metastases: rationale and preclinical studies.Cancer letters · 2010Review
- The tumor suppressor functions of p27(kip1) include control of the mesenchymal/amoeboid transition.Molecular and cellular biology · 2009Article
- Identification and functional signature of genes regulated by structurally different ABL kinase inhibitors.Oncogene · 2007Article
- RACK1 inhibits colonic cell growth by regulating Src activity at cell cycle checkpoints.Oncogene · 2007Article
- Article
- Peptide modulators of Src activity in G1 regulate entry into S phase and proliferation of NIH 3T3 cells.Biochemical and biophysical research communications · 2007Article
- Increases in c-Src expression level and activity do not promote the growth of human colorectal carcinoma cells in vitro and in vivo.Neoplasia (New York, N.Y.) · 2006Article
- Activated Src abrogates the Myc requirement for the G0/G1 transition but not for the G1/S transition.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Active Src elevates the expression of beta-catenin by enhancement of cap-dependent translation.Molecular and cellular biology · 2005Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tyrosine kinase oncoprotein v-Src can overcome the requirements for serum growth factors and anchorage which restrain normal cell growth. Here we investigated the biochemical mechanisms whereby v-Src induces quiescent cells to enter S phase in the absence of serum mitogens. Activating a temperature sensitive v-Src in quiescent cells sequentially induced cyclins D1, E and A and also down regulated p27. We addressed whether p27 down regulation was required to activate cyclin D1/CDK4/6 or cyclin E/CDK2 by engineering cells with inducible p27. Both S phase entry and activation of cyclin/CDKs were inhibited by over expression of p27. Using cells engineered with inducible p16 we showed that Cyclin D/CDK4/6 activity was required for v-Src to increase expression of cyclin A but not cyclin E. To determine which downstream kinases mediated these effects of v-Src we added pharmacological inhibitors of phosphatidylinositol 3-kinase (PI3-K), LY294002 or mitogen activated protein kinase kinase (MEK), U0126. PI3-K was required for v-Src to activate MEK and MEK was required for v-Src to increase expression of cyclins D1 and E. However, the MEK inhibitor prevented p27 protein down regulation whereas the PI3-K inhibitor did not. This was because reduced PI3-K activity lead to proteolytic degradation of p27.
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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.