ArticleMolecular biology international2012
Loss of RASSF2 Enhances Tumorigencity of Lung Cancer Cells and Confers Resistance to Chemotherapy.
Article in Molecular biology international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- PACT is requisite for prostate cancer cell proliferation.Scientific reports · 2025Article
- Identification and characterization of biomarkers and their functions for Lapatinib-resistant breast cancer.Medical oncology (Northwood, London, England) · 2017Article
- Cancer-associated fibroblasts promote cancer cell growth through a miR-7-RASSF2-PAR-4 axis in the tumor microenvironment.Oncotarget · 2017Article
- Ras signaling through RASSF proteins.Seminars in cell & developmental biology · 2016Review
- miEAA: microRNA enrichment analysis and annotation.Nucleic acids research · 2016Article
- Article
- Lung cancer in which the hypothesis of multi-step progression is confirmed by array-CGH results: A case report.Experimental and therapeutic medicine · 2016Article
- Differential involvement of RASSF2 hypermethylation in breast cancer subtypes and their prognosis.Oncotarget · 2015Article
- Cell cycle restriction is more important than apoptosis induction for RASSF1A protein tumor suppression.The Journal of biological chemistry · 2014Article
- RASSF2 methylation is a strong prognostic marker in younger age patients with Ewing sarcoma.Epigenetics · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RASSF2 is a novel pro-apoptotic effector of K-Ras that is frequently inactivated in a variety of primary tumors by promoter methylation. Inactivation of RASSF2 enhances K-Ras-mediated transformation and overexpression of RASSF2 suppresses tumor cell growth. In this study, we confirm that RASSF2 and K-Ras form an endogenous complex, validating that RASSF2 is a bona fide K-Ras effector. We adopted an RNAi approach to determine the effects of inactivation of RASSF2 on the transformed phenotype of lung cancer cells containing an oncogenic K-Ras. Loss of RASSF2 expression resulted in a more aggressive phenotype that was characterized by enhanced cell proliferation and invasion, decreased cell adhesion, the ability to grow in an anchorage-independent manner and cell morphological changes. This enhanced transformed phenotype of the cells correlated with increased levels of activated AKT, indicating that RASSF2 can modulate Ras signaling pathways. Loss of RASSF2 expression also confers resistance to taxol and cisplatin, two frontline therapeutics for the treatment of lung cancer. Thus we have shown that inactivation of RASSF2, a process that occurs frequently in primary tumors, enhances the transforming potential of activated K-Ras and our data suggests that RASSF2 may be a novel candidate for epigenetic-based therapy in lung cancer.
Identifiers
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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.