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

• Grant number: 16/17945-6
• Support Opportunities: Scholarships abroad - Research Internship - Post-doctor
• Start date: November 30, 2016
• End date: November 29, 2017
• Field of knowledge: Biological Sciences - Biochemistry - Molecular Biology
• Principal Investigator: Hugo Aguirre Armelin
• Grantee: Matheus Henrique dos Santos Dias
• Supervisor: Ian Prior
• Host Institution: Instituto Butantan. Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
• Institution abroad: 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

Abstract

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.; et al. Fibroblast Growth Factor 2 lethally sensitizes cancer cells to stress-targeted therapeutic inhibitors. MOLECULAR ONCOLOGY, v. 13, n. 2, p. 17-pg., 2019-02-01. (16/17945-6, 13/09040-5, 12/20186-9, 13/24212-7)

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.; et al. Fibroblast Growth Factor 2 lethally sensitizes cancer cells to stress-targeted therapeutic inhibitors. MOLECULAR ONCOLOGY, v. 13, n. 2, p. 290-306, FEB 2019. (12/20186-9, 13/09040-5, 13/24212-7, 16/17945-6)