ArticleMolecular and cellular biology2008
Anchorage-independent growth of pocket protein-deficient murine fibroblasts requires bypass of G2 arrest and can be accomplished by expression of TBX2.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Development of an integrated testing strategy using in vitro models to predict lung carcinogenesis.Environmental analysis, health and toxicology · 2025Article
- Restoring the DREAM Complex Inhibits the Proliferation of High-Risk HPV Positive Human Cells.Cancers · 2021Article
- Genetic status of KRAS influences Transforming Growth Factor-beta (TGF-β) signaling: An insight into Neuropilin-1 (NRP1) mediated tumorigenesis.Seminars in cancer biology · 2019Review
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- Metallic nickel nanoparticles may exhibit higher carcinogenic potential than fine particles in JB6 cells.PloS one · 2014Article
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- A pathway for the control of anoikis sensitivity by E-cadherin and epithelial-to-mesenchymal transition.Molecular and cellular biology · 2011Article
- Ras-induced senescence and its physiological relevance in cancer.Current cancer drug targets · 2010Review
- TBX2 and TBX3: the special value for anticancer drug targets.Biochimica et biophysica acta · 2010Review
- The retinoblastoma protein modulates Tbx2 functional specificity.Molecular biology of the cell · 2010Article
- Loss of Rb proteins causes genomic instability in the absence of mitogenic signaling.Genes & development · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse embryonic fibroblasts (MEFs) deficient for pocket proteins (i.e., pRB/p107-, pRB/p130-, or pRB/p107/p130-deficient MEFs) have lost proper G(1) control and are refractory to Ras(V12)-induced senescence. However, pocket protein-deficient MEFs expressing Ras(V12) were unable to exhibit anchorage-independent growth or to form tumors in nude mice. We show that depending on the level of pocket proteins, loss of adhesion induces G(1) and G(2) arrest, which could be alleviated by overexpression of the TBX2 oncogene. TBX2-induced transformation occurred only in the absence of pocket proteins and could be attributed to downregulation of the p53/p21(CIP1) pathway. Our results show that a balance between the pocket protein and p53 pathways determines the level of transformation of MEFs by regulating cyclin-dependent kinase activities. Since transformation of human fibroblasts also requires ablation of both pathways, our results imply that the mechanisms underlying transformation of human and mouse cells are not as different as previously claimed.
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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.