ArticleMolecular and cellular biology2013
The differential effects of wild-type and mutated K-Ras on MST2 signaling are determined by K-Ras activation kinetics.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Rac1 GTPase Regulates the βTrCP-Mediated Proteolysis of YAP Independently of the LATS1/2 Kinases.Cancers · 2024Article
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- Dynamic regulation of RAS and RAS signaling.The Biochemical journal · 2023Article
- Interaction of LATS1 with SMAC links the MST2/Hippo pathway with apoptosis in an IAP-dependent manner.Cell death & disease · 2022Article
- Loss of the wild-type KRAS allele promotes pancreatic cancer progression through functional activation of YAP1.Oncogene · 2021Article
- Resistance to Targeted Therapy and RASSF1A Loss in Melanoma: What Are We Missing?International journal of molecular sciences · 2021Review
- Article
- Characterisation of HRas local signal transduction networks using engineered site-specific exchange factors.Small GTPases · 2020Article
- Review
- The Hippo pathway integrates PI3K-Akt signals with mechanical and polarity cues to control tissue growth.PLoS biology · 2019Article
- Article
- Novel β-phenylacrylic acid derivatives exert anti-cancer activity by inducing Src-mediated apoptosis in wild-type KRAS colon cancer.Cell death & disease · 2018Article
- Hras helps hippo heterodimerize to evade tumor suppression.Small GTPases · 2018Review
- RASSF1A Deficiency Enhances RAS-Driven Lung Tumorigenesis.Cancer research · 2018Article
- Mitochondrial determinants of cancer health disparities.Seminars in cancer biology · 2017Review
- Racial disparity in metabolic regulation of cancer.Frontiers in bioscience (Landmark edition) · 2017Review
- Mutant allele specific imbalance in oncogenes with copy number alterations: Occurrence, mechanisms, and potential clinical implications.Cancer letters · 2017Review
- H-ras Inhibits the Hippo Pathway by Promoting Mst1/Mst2 Heterodimerization.Current biology : CB · 2016Article
- Review
- Rare codons capacitate Kras-driven de novo tumorigenesis.The Journal of clinical investigation · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
K-Ras is frequently mutated in human cancers. Mutant (mt) K-Ras can stimulate both oncogenic transformation and apoptosis through activation of extracellular signal-regulated kinase (ERK) and AKT pathways and the MST2 pathway, respectively. The biological outcome is determined by the balance and cross talk between these pathways. In colorectal cancer (CRC), a K-Ras mutation is negatively correlated with MST2 expression, as mt K-Ras can induce apoptosis by activating the MST2 pathway. However, wild-type (wt) K-Ras can prevent the activation of the MST2 pathway upon growth factor stimulation and enable transformation by mt K-Ras in CRC cells that express MST2. Here we have investigated the mechanism by which wt and mt K-Ras differentially regulate the MST2 pathway and MST2-dependent apoptosis. The ability of K-Ras to activate MST2 and MST2-dependent apoptosis is determined by the differential activation kinetics of mt K-Ras and wt K-Ras. Chronic activation of K-Ras by mutation or overexpression of Ras exchange factors results in the activation of MST2 and LATS1, increased MST2-LATS1 complex formation, and apoptosis. In contrast, transient K-Ras activation upon epidermal growth factor (EGF) stimulation prevents the formation of the MST2-LATS1 complex in an AKT-dependent manner. Our data suggest that the close relationship between Ras prosurvival and proapoptotic signaling is coordinated via the differential regulation of the MST2-LATS1 interaction by transient and chronic stimuli.
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