Jenifer Saffi

Universidade Federal de Ciências da Saúde de Porto Alegre, Ciências Básicas da Saúde, Faculty Member

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Phamacist, PhD in Biochemistry (1999) by the Federal University of Rio Grande do Sul (UFRGS)- Porto Alegre- Brazil and Post-Doc at the “Institut de Cancérologie Gustave Roussy” in Villejuif – France (2007-2008). Biochemisty Professor at the Federal University of Health Sciences of Porto Alegre (UFCSPA) since 2009. Vice-rector at UFCSPA (2017-2021; 2021-2025) and Head of the Internationalization Office. Coordinator of the Laboratory of Genetic Toxicology. Her main research area is DNA repair and mutagenesis in eukaryotic cells, focusing on the involvement of the DNA repair mechanisms in the cytotoxicity of antitumor drugs and DNA damage response in cancer, presenting more than 100 international papers published in the field. She was a member of the National Committee of Biosafety (CTNBio – Brazil; 2014-2020).

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Determinação dos potenciais cicatrizante e anti-inflamatório de um extrato hidroetanólico de plantago australis (KUNTH) rahn e do seu constituinte verbascosídeo, utilizando modelos in vitro

Doxorubicin induced killing in cells deficient in different DNA repair pathways

A novel 1-((3-(2-toluyl)-4,5-dihydroisoxazol-5-yl)methyl)-4-(trifluoromethyl)pyrimidin-2(1H)-one activates intrinsic mitochondria-dependent pathway and decreases angiogenesis in PC-3 cells

European Journal of Pharmacology, 2021

Prostate cancer is among the most common cancer diagnoses in men, and the best treatment for pati... more Prostate cancer is among the most common cancer diagnoses in men, and the best treatment for patients with metastatic disease in advanced stages is still unclear. Previously, we have demonstrated that the three 1-(3-(aryl-4,5-dihydroisoxazol-5-yl)methyl)-4-trihalomethyl-1H-pyrimidin-2- ones derivatives (8a, 8e and 9c) present important cytotoxicity and selectivity for tumoral cells. Considering that various cytotoxic drugs have been assessed in patients with prostate cancer, but few drugs show survival advantage, we decided to study these three compounds (8a, 8e and 9c) in prostate cancer cells, androgen receptor (AR)-positive 22Rv-1 and AR-negative PC-3 cells. We obtained the half maximal inhibitory concentration (IC50) of 8a, 8e and 9c in prostate cancer cells and based on high selectivity of 9c to PC-3 cells, we determined the mechanism of this compound to induce cell death through different methods. We show here that 9c compound induces cell cycle arrest in G2/M, increasing the levels of reactive oxygen species and DNA damage, and triggers DNA damage response by ataxia-telangiectasia mutated (ATM) and histone H2AX phosphorylation induction. The compound also led PC-3 to lipid peroxidation and mitochondrial depolarization which triggered the activation of intrinsic pathway, confirmed by increase of cleaved caspase-9 and 3. In this work we also show the ability of 9c in reducing vascular endothelial growth factor expression (VEGF) and inhibiting topoisomerase I enzyme, therefore indicating a potential new molecule to be further investigated for prostate cancer management.

Olaparib-mediated enhancement of 5-fluorouracil cytotoxicity in mismatch repair deficient colorectal cancer cells

BMC Cancer, 2021

Background The advances in colorectal cancer (CRC) treatment include the identification of defici... more Background The advances in colorectal cancer (CRC) treatment include the identification of deficiencies in Mismatch Repair (MMR) pathway to predict the benefit of adjuvant 5-fluorouracil (5-FU) and oxaliplatin for stage II CRC and immunotherapy. Defective MMR contributes to chemoresistance in CRC. A growing body of evidence supports the role of Poly-(ADP-ribose) polymerase (PARP) inhibitors, such as Olaparib, in the treatment of different subsets of cancer beyond the tumors with homologous recombination deficiencies. In this work we evaluated the effect of Olaparib on 5-FU cytotoxicity in MMR-deficient and proficient CRC cells and the mechanisms involved. Methods Human colon cancer cell lines, proficient (HT29) and deficient (HCT116) in MMR, were treated with 5-FU and Olaparib. Cytotoxicity was assessed by MTT and clonogenic assays, apoptosis induction and cell cycle progression by flow cytometry, DNA damage by comet assay. Adhesion and transwell migration assays were also performed...

Jenifer Saffi

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