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Proteome/phosphoproteome networks investigation of the complementary role of Cyclin D1 for Ras-driven malignant transformation

Grant number: 16/17945-6
Support type:Scholarships abroad - Research Internship - Post-doctor
Effective date (Start): November 30, 2016
Effective date (End): November 29, 2017
Field of knowledge:Biological Sciences - Biochemistry
Principal Investigator:Hugo Aguirre Armelin
Grantee:Matheus Henrique dos Santos Dias
Supervisor abroad: Ian Prior
Home Institution: Instituto Butantan. Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
Local de pesquisa : University of Liverpool, England  
Associated to the scholarship:12/20186-9 - Molecular mechanisms of functional interaction between Ras and cyclin D1 in Ras-driven malignant cells, BP.PD


We propose that in Ras-driven malignant cells there is a functional interaction between cyclin D1 and this oncogene; in which the main function of cyclin D1 is to guarantee cell survival overcoming the Ras oncogenic stress. We showed in the presented reports that CRISPR-Cas9-mediated cyclin D1 depletion induces p53-independent senescence in Ras-driven carcinoma cells. Moreover, in MEFs cyclin D1 overexpression attenuates Ras-induced oncogenic stress enabling cell viability and proliferation. Elucidation of the molecular mechanisms underlying this putative functional interaction between Ras and cyclin D1 is the central goal of this project. These issues will be addressed by proteome and phosphoproteome network analyses followed by validation of key proteins involved in these molecular mechanisms. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
DIAS, MATHEUS H.; FONSECA, CECILIA S.; ZEIDLER, JULIANNA D.; ALBUQUERQUE, LAYRA L.; DA SILVA, MARCELO S.; CARARO-LOPES, EDUARDO; REIS, MARCELO S.; NOEL, VINCENT; DOS SANTOS, EDMILSON O.; PRIOR, IAN A.; ARMELIN, HUGO A. Fibroblast Growth Factor 2 lethally sensitizes cancer cells to stress-targeted therapeutic inhibitors. MOLECULAR ONCOLOGY, v. 13, n. 2, p. 290-306, FEB 2019. Web of Science Citations: 0.

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