ArticleMolecular and cellular biology2006
The retinoblastoma protein is required for Ras-induced oncogenic transformation.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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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
31 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Unraveling the Genetic Web: H-Ras Expression and Mutation in Oral Squamous Cell Carcinoma-A Systematic Review.Head and neck pathology · 2024Pooled it
- P16iScience · 2024Article
- Indolium 1 Exerts Activity against Vemurafenib-Resistant Melanoma In Vivo.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- NRAS Contributes to Retinoblastoma Progression Through SNHG16/miR-183-5p/NRAS Regulatory Network.OncoTargets and therapy · 2019Article
- Analysis of mutation, selection, and epistasis: an informed approach to cancer clinical trials.Oncotarget · 2018Article
- Select human cancer mutants of NRMT1 alter its catalytic activity and decrease N-terminal trimethylation.Protein science : a publication of the Protein Society · 2017Article
- Bioinformatic identification of prognostic signature defined by copy number alteration and expression of CCNE1 in non-muscle invasive bladder cancer.Experimental & molecular medicine · 2017Article
- Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies.World journal of stem cells · 2016Review
- Germline mutations in oncogene-induced senescence pathways are associated with multiple sessile serrated adenomas.Gastroenterology · 2014Article
- Article
- Posttranslational modifications of the retinoblastoma tumor suppressor protein as determinants of function.Genes & cancer · 2012Article
- Twists in views on RB functions in cellular signaling, metabolism and stem cells.Cancer science · 2012Review
- A dual role for the dREAM/MMB complex in the regulation of differentiation-specific E2F/RB target genes.Molecular and cellular biology · 2012Article
- The retinoblastoma family of proteins and their regulatory functions in the mammalian cell division cycle.Cell division · 2012Article
- Targeting protein prenylation for cancer therapy.Nature reviews. Cancer · 2011Article
- Deletion of Rb accelerates pancreatic carcinogenesis by oncogenic Kras and impairs senescence in premalignant lesions.Gastroenterology · 2011Article
- Potent anti-tumor effect generated by a novel human papillomavirus (HPV) antagonist peptide reactivating the pRb/E2F pathway.PloS one · 2011Article
- RB1, development, and cancer.Current topics in developmental biology · 2011Review
- Modeling the effect of the RB tumor suppressor on disease progression: dependence on oncogene network and cellular context.Oncogene · 2010Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most human cancers involve either mutational activation of the Ras oncogenic pathway and/or inactivation of the retinoblastoma tumor suppressor (RB) pathway. Paradoxically, tumors that harbor Ras mutations almost invariably retain expression of a wild-type pRB protein. We explain this phenomenon by demonstrating that Ras-induced oncogenic transformation surprisingly depends on functional pRB protein. Cells lacking pRB are less susceptible to the oncogenic actions of H-RasV12 than wild-type cells and activated Ras has an inhibitory effect on the proliferation of pRB-deficient human tumor cells. In addition, depletion of pRB from Ras-transformed murine cells or human tumor cells that harbor Ras pathway mutations inhibits their proliferation and anchorage-independent growth. In sharp contrast to pRB-/- 3T3 cells, fibroblasts deficient in other pRB family members (p107 and p130) are more susceptible to Ras-mediated transformation than wild-type 3T3 cells. Moreover, loss of pRB in tumor cells harboring a Ras mutation results in increased expression of p107, and overexpression of p107 but not pRB strongly inhibits proliferation of these tumor cells. Together, these findings suggest that pRB and p107 have distinct roles in Ras-mediated transformation and suggest a novel tumor-suppressive role for p107 in the context of activated Ras.
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