Proceedings of Oncobiology Symposiums
Proceedings of XIV Oncobiology Symposium

INTRODUCTION AND OBJECTIVES: Breast cancer (BC) is the most common cancer diagnosed worldwide in women. The mortality of BC is mainly caused by metastases development. Apurinic/apyrimidinic endonuclease 1 (APE1) is a dual-function protein; it has an important role in the base excision repair (BER) pathway and provides, in response to the redox metabolism, activation of multiple transcription factors. APE1 expression and protein activity have been associated with more aggressive tumor phenotypes and poor prognosis. Therefore, this study aimed to evaluate the effects of APE1 redox domain inhibition, by APX2009, on the malignant phenotype of MDA-MB-231 BC cell line. MATERIAL AND METHODS: WST1 (water-soluble tetrazolium) and Colony formation test were used to evaluate cell proliferation. To measure the potential migration of cancer cells, the wound healing (WH) test was carried out by cell monolayers were wounded by scratching them, incubated culture medium 1% SFB, images were collected at 0h and 24h, and migratory characteristics were evaluated comparing APX2009 treated versus untreated cells. Matrigel transwell invasion was performed, and after 24h incubation, cells were fixed and stained with crystal violet, random fields were photographed and counted. RESULTS AND CONCLUSION: Cell proliferation assay showed toxicity induction after 24h at concentrations 20μM and 100μM, resulting in 55% of cell survival compared to control. For colony formation assay, 4μM significantly reduces the colony number. Non-toxic concentrations were used in WH and invasion assays, and the results show that treatment at 4μM significantly reduces the invasiveness potential of MDA-MB-231 cells. However, no alteration in cellular migration had been observed. These results suggest that the inhibitor of APE1 redox signaling, APX2009, may have some influence on the malignant potential of triple-negative breast cancer cells.