Induction of apoptosis or cell proliferation in breast and prostate tumor cell lines by the novel cytokine PANDER

• Grant number: 07/04513-1
• Support type: Regular Research Grants
• Duration: December 01, 2007 - November 30, 2008
• Field of knowledge: Biological Sciences - Biochemistry - Molecular Biology
• Principal Investigator: Humberto Miguel Garay Malpartida
• Grantee: Humberto Miguel Garay Malpartida
• Home Institution: Escola de Artes, Ciências e Humanidades (EACH). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

The PANDER/FAM3B (pancreatic-derived factor) was recently identified as a novel cytokine expressed almost exclusively by the pancreatic islets. It was demonstrated that PANDER induces apoptosis in insulin secreting beta-cells. However, our in silico data revealed that the PANDER gene is also expressed in prostate and breast tumors. Our goal is to evaluate the functional role of PANDER in tumor cell lines by means of: 1) lentiviral-mediated overexpression of PANDER gene and 2) post-transcriptional gene silencing mediated by RNA interference. The ability of PANDER to induce apoptosis and/or proliferation will be evaluated. The proliferative rate will be measured by DNA synthesis and cell viability quantitative assays. The apoptosis occurrence will be evaluated by DNA fragmentation analysis, changes in cell membrane, caspase activity and apoptosis-related gene expression. We hope these results can direct future efforts to better understand the functional role of this novel cytokine in the control of tumoral progression. (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)

MACIEL-SILVA, PAULA; CALDEIRA, IZABELA; SANTOS, ICARO DE ASSIS; OLIVEIRA CARREIRA, ANA CLAUDIA; SIQUEIRA, FLAVIA RAMOS; ANTONIOLI, ELIANE; GOLDBERG, ANNA CARLA; BELIZARIO, JOSE ERNESTO; GARAY-MALPARTIDA, HUMBERTO MIGUEL. FAM3B/PANDER inhibits cell death and increases prostate tumor growth by modulating the expression of Bcl-2 and Bcl-X-L cell survival genes. BMC CANCER, v. 18, JAN 22 2018. Web of Science Citations: 3.

BELIZARIO, JOSE E.; FAINTUCH, JOEL; GARAY-MALPARTIDA, MIGUEL. Gut Microbiome Dysbiosis and Immunometabolism: New Frontiers for Treatment of Metabolic Diseases. Mediators of Inflammation, 2018. Web of Science Citations: 11.