ArticleThe Journal of biological chemistry2014
Ral GTPase down-regulation stabilizes and reactivates p53 to inhibit malignant transformation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- c-Jun N-terminal kinase signaling in cellular senescence.Archives of toxicology · 2023Review
- Antitumor Effects of Ral-GTPases Downregulation in Glioblastoma.International journal of molecular sciences · 2022Article
- Presence of serum RalA and serum p53 autoantibodies in 1833 patients with various types of cancers.International journal of clinical oncology · 2022Article
- Ral GTPase is essential for actin dynamics and Golgi apparatus distribution in mouse oocyte maturation.Cell division · 2021Article
- Targeting K-Ras and apoptosis-driven cellular transformation in cancer.Cell death discovery · 2021Review
- Lysine Fatty Acylation: Regulatory Enzymes, Research Tools, and Biological Function.Frontiers in cell and developmental biology · 2021Review
- RALB GTPase: a critical regulator of DR5 expression and TRAIL sensitivity in KRAS mutant colorectal cancer.Cell death & disease · 2020Article
- The GTPase KRAS suppresses the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells.The Journal of biological chemistry · 2020Article
- SIRT2 and Lysine Fatty Acylation Regulate the Activity of RalB and Cell Migration.ACS chemical biology · 2019Article
- Using recursive partitioning approach to select tumor-associated antigens in immunodiagnosis of gastric adenocarcinoma.Cancer science · 2019Article
- Cathepsin F Knockdown Induces Proliferation and Inhibits Apoptosis in Gastric Cancer Cells.Oncology research · 2018Article
- Ral signaling pathway in health and cancer.Cancer medicine · 2017Review
- Brusatol overcomes chemoresistance through inhibition of protein translation.Molecular carcinogenesis · 2017Article
- A genome-wide siRNA screen for regulators of tumor suppressor p53 activity in human non-small cell lung cancer cells identifies components of the RNA splicing machinery as targets for anticancer treatment.Molecular oncology · 2017Article
- Hypoxic resistance of KRAS mutant tumor cells to 3-Bromopyruvate is counteracted by Prima-1 and reversed by N-acetylcysteine.BMC cancer · 2016Article
- Analysis of Microarray Data on Gene Expression and Methylation to Identify Long Non-coding RNAs in Non-small Cell Lung Cancer.Scientific reports · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ral GTPases are critical effectors of Ras, yet the molecular mechanism by which they induce malignant transformation is not well understood. In this study, we found the expression of K-Ras, RalB, and sometimes RalA, but not AKT1/2 and c-Raf, to be required for maintaining low levels of p53 in human cancer cells that harbor mutant K-Ras and wild-type p53. Down-regulation of K-Ras, RalB, and sometimes RalA increases p53 protein levels and results in a p53-dependent up-regulation of the expression of p21(WAF). K-Ras, RalA, and RalB depletion increases p53 stability as demonstrated by ataxia telangiectasia-mutated kinase activation, increased Ser-15 phosphorylation, and a significant (up to 6-fold) increase in p53 half-life. Furthermore, depletion of K-Ras and RalB inhibits anchorage-independent growth and invasion and interferes with cell cycle progression in a p53-dependent manner. Depletion of RalA inhibits invasion in a p53-dependent manner. Thus, expression of K-Ras and RalB and possibly RalA proteins is critical for maintaining low levels of p53, and down-regulation of these GTPases reactivates p53 by significantly enhancing its stability, and this contributes to suppression of malignant transformation.
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