ArticleMolecular and cellular biology2014
RASSF1A inactivation unleashes a tumor suppressor/oncogene cascade with context-dependent consequences on cell cycle progression.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Aberrant promoter methylation, expression and function of RASSF1A gene in a series of Italian parathyroid tumors.Endocrine · 2025Article
- Epigenetics in thyroid cancer: a bibliometric analysis.Endocrine connections · 2024Article
- Diagnostic performance of RASSF1A and SHOX2 methylation combined with EGFR mutations for differentiation between small pulmonary nodules.Journal of cancer research and clinical oncology · 2023Article
- The Diagnostic Potential ofFrontiers in oncology · 2022Article
- Signaling pathways and clinical application of RASSF1A and SHOX2 in lung cancer.Journal of cancer research and clinical oncology · 2020Review
- The Role and Function of Ras-association domain family in Cancer: A Review.Genes & diseases · 2019Review
- Article
- Tumor suppressor C-RASSF proteins.Cellular and molecular life sciences : CMLS · 2018Review
- Local Delivery of miR-21 Stabilizes Fibrous Caps in Vulnerable Atherosclerotic Lesions.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Relationship between the Methylation of Folic Acid Metabolism-Related Genes and the Incidence and Prognosis of Esophageal Cancer among Ethnic Kazakhs.Journal of Cancer · 2018Article
- miR-1908 as a novel prognosis marker of glioma via promoting malignant phenotype and modulating SPRY4/RAF1 axis.Oncology reports · 2017Article
- The role of the NORE1A tumor suppressor in Oncogene-Induced Senescence.Cancer letters · 2017Review
- Ras signaling through RASSF proteins.Seminars in cell & developmental biology · 2016Review
- Surgical and molecular pathology of pancreatic neoplasms.Diagnostic pathology · 2016Review
- Methylation of RASSF1A gene promoter and the correlation with DNMT1 expression that may contribute to esophageal squamous cell carcinoma.World journal of surgical oncology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The RASSF1A gene is one of the most frequently inactivated genes in over 30 different types of cancers (H. Donninger, M. D. Vos, and G. J. Clark, J. Cell Sci. 120:3163-3172, 2007, http://dx.doi.org/10.1242/jcs.010389). Despite the prevalence of RASSF1A silencing in human cancer, the mechanism by which RASSF1A functions as a tumor suppressor is not well understood. Characterization of the consequences of RASSF1A loss on epithelial cell proliferation revealed that RASSF1A expression suppresses both microRNA 21 (miR-21) expression and extracellular signal-regulated kinase 1/2 (ERK1/2) activation. The mechanism of the former is through restraint of SCF(βTrCP)-dependent destruction of the repressor element 1 silencing transcription factor (REST) tumor suppressor and consequent inhibition of miR-21 promoter activation. The mechanism of the latter is through physical sequestration of MST2, which results in accumulation of inactivating S259 phosphorylation of RAF1. Whether or not inactivation of these RASSF1A regulatory relationships can unleash enhanced proliferative capacity is dependent upon the coupling of SCF(βTrCP) and miR-21 to suppression of SKP2 protein translation and stability. Airway epithelial cultures retain this coupling and therefore respond to RASSF1A inactivation by p27-dependent cell cycle arrest. In contrast, colonic crypt-derived epithelial cells have uncoupled SCF(βTrCP) from SKP2 and respond to RASSF1A inactivation by enhanced proliferation rates. These observations help account for context-specific molecular etiology of oncogenic transformation and suggest intervention strategies for recently developed SKP2 inhibitors.
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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.