ArticleProceedings of the National Academy of Sciences of the United States of America2006
Activated Src abrogates the Myc requirement for the G0/G1 transition but not for the G1/S transition.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
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- EZH2 synergizes with BRD4-NUT to drive NUT carcinoma growth through silencing of key tumor suppressor genes.bioRxiv : the preprint server for biology · 2023Article
- microRNA-205 in prostate cancer: Overview to clinical translation.Biochimica et biophysica acta. Reviews on cancer · 2022Review
- MAP9 Exhibits Protumor Activities and Immune Escape toward Bladder Cancer by Mediating TGF-Journal of oncology · 2022Article
- Targeting MYC in multiple myeloma.Leukemia · 2018Review
- βArrestin2 Mediates Renal Cell Carcinoma Tumor Growth.Scientific reports · 2018Article
- Effects of LG268 on Cell Proliferation and Apoptosis of NB4 Cells.International journal of medical sciences · 2016Article
- Mitochondrial ribosomal protein S18-2 evokes chromosomal instability and transforms primary rat skin fibroblasts.Oncotarget · 2015Article
- Src kinase function controls progenitor cell pools during regeneration and tumor onset in the Drosophila intestine.Oncogene · 2015Article
- MYC and the control of DNA replication.Cold Spring Harbor perspectives in medicine · 2014Review
- miR-205 is frequently downregulated in prostate cancer and acts as a tumor suppressor by inhibiting tumor growth.Asian journal of andrology · 2013Article
- miR-23b represses proto-oncogene Src kinase and functions as methylation-silenced tumor suppressor with diagnostic and prognostic significance in prostate cancer.Cancer research · 2012Article
- Human Breast Cancer Stem Cells Have Significantly Higher Rate of Clathrin-Independent and Caveolin-Independent Endocytosis than the Differentiated Breast Cancer Cells.Journal of cancer science & therapy · 2012Article
- MicroRNA-205 inhibits Src-mediated oncogenic pathways in renal cancer.Cancer research · 2011Article
- p27Kip1 mediates addiction of ovarian cancer cells to MYCC (c-MYC) and their dependence on MYC paralogs.The Journal of biological chemistry · 2010Article
- SRC: a century of science brought to the clinic.Neoplasia (New York, N.Y.) · 2010Review
- Stabilizers of the Max homodimer identified in virtual ligand screening inhibit Myc function.Molecular pharmacology · 2009Article
- Influence of the Circadian System on Disease Severity.Sleep medicine clinics · 2009Article
- Src family kinase oncogenic potential and pathways in prostate cancer as revealed by AZD0530.Oncogene · 2008Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factor Myc plays a central role in the control of cellular proliferation. Myc expression is induced by growth factors in a pathway mediated by cellular Src (c-Src), but it is not clear whether Myc induction or activity is required for malignant transformation by activated Src. We introduced v-Src into a c-myc(-/-) derivative of Rat-1 fibroblasts and into 3T9 mouse fibroblasts harboring a conditionally excisable c-myc allele. Expression of activated viral Src in Myc-deficient cells led to loss of actin stress fibers and surface fibronectin, indicating that Myc is dispensable for v-Src-induced morphological transformation. However, v-Src failed to rescue the proliferative defect resulting from the loss of Myc. In Myc-deficient cells, despite its inability to overcome this proliferation block, v-Src was able to regulate the expression of certain Myc transcriptional targets and induce the expression of active cyclin D/Cdk4 and Cdk6 complexes; it also induced the phosphorylation of Rb, albeit at reduced levels. In contrast, however, in the absence of Myc, the level of Cdk2 kinase activity was drastically reduced. This reduction in Cdk2 activity was associated with a decrease in the expression of Cdk7, Cdc25A, and cyclin A. Coexpression of Cdk2 plus cyclin E and/or cyclin A rescued the G1/S block and allowed the cells to enter mitosis. These results indicate that in the absence of Myc, v-Src can activate early G1 cell cycle regulators but fails to activate regulators of the late G1/S transition.
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