ArticleOncogene2002
Raf-1-induced growth arrest in human mammary epithelial cells is p16-independent and is overcome in immortal cells during conversion.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed.
- Inhibition of protein kinase C delta leads to cellular senescence to induce anti-tumor effects in colorectal cancer.Cancer science · 2023Article
- IL1 Pathway in HPV-Negative HNSCC Cells Is an Indicator of Radioresistance After Photon and Carbon Ion Irradiation Without Functional Involvement.Frontiers in oncology · 2022Article
- Kinesin Family Member C1 (KIFC1/HSET): A Potential Actionable Biomarker of Early Stage Breast Tumorigenesis and Progression of High-Risk Lesions.Journal of personalized medicine · 2021Review
- Chemotherapy Induces Senescence-Like Resilient Cells Capable of Initiating AML Recurrence.Cancer discovery · 2021Article
- The Histone Code of Senescence.Cells · 2020Review
- Nuclear receptor HNF4α performs a tumor suppressor function in prostate cancer via its induction of p21-driven cellular senescence.Oncogene · 2020Article
- Experimental identification of cancer driver alterations in the era of pan-cancer genomics.Cancer science · 2019Review
- Ell3 functions as a critical decision maker at the crossroad between stem cell senescence and apoptosis.Stem cell research & therapy · 2019Article
- Breast Tissue Biology Expands the Possibilities for Prevention of Age-Related Breast Cancers.Frontiers in cell and developmental biology · 2019Review
- The Neuro-Immuno-Senescence Integrative Model (NISIM) on the Negative Association Between Parasympathetic Activity and Cellular Senescence.Frontiers in neuroscience · 2018Article
- Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?Cellular and molecular life sciences : CMLS · 2017Review
- Redox control of senescence and age-related disease.Redox biology · 2017Review
- STAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence.Cell cycle (Georgetown, Tex.) · 2017Article
- Multiple facets of p53 in senescence induction and maintenance.Cancer science · 2016Review
- The Intricate Interplay between Mechanisms Underlying Aging and Cancer.Aging and disease · 2015Review
- Article
- Exome-wide mutation profile in benzo[a]pyrene-derived post-stasis and immortal human mammary epithelial cells.Mutation research. Genetic toxicology and environmental mutagenesis · 2014Article
- Growth arrest signaling of the Raf/MEK/ERK pathway in cancer.Frontiers in biology · 2014Article
- Initiation of premature senescence by Bcl-2 in hypoxic condition.International journal of clinical and experimental pathology · 2014Article
- Immortalization of normal human mammary epithelial cells in two steps by direct targeting of senescence barriers does not require gross genomic alterations.Cell cycle (Georgetown, Tex.) · 2014Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Using an estrogen-inducible retroviral system, we demonstrate that oncogenic Raf-1 induces growth arrest and morphological changes in finite lifespan human mammary epithelial cells (HMEC). This arrest does not rely on expression of the cyclin-dependent kinase inhibitor (CKI) p16(INK4a), nor on changes in expression of the CKIs p21(Cip1), p14(ARF), p27(Kip1) or p57(Kip2). The Raf-induced arrest is independent of viral oncogene mediated inactivation of p53 and pRB, or c-myc overexpression. Flow cytometric analysis demonstrates that cells arrest in both G1 and G2. The Raf-induced arrest is mitigated or eliminated in some immortally transformed HMEC. Immortal HMEC that have both overcome replicative senescence and undergone the recently described conversion process maintain growth in the presence of transduced oncogenic Raf-1; they also gain EGF-independent growth and a low frequency of anchorage-independent growth. However, HMEC that have overcome replicative senescence but have not undergone conversion and HMEC immortalized by transduction with the catalytic subunit of telomerase, hTERT, remain severely growth arrested. These results indicate that the molecular mechanisms responsible for the Raf-1-induced growth arrest may vary among different finite lifespan cell types, and that in HMEC, this mechanism is altered during the conversion process, rather than as a direct consequence of overcoming senescence or expressing hTERT.
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Registered trials
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