Abstract
Prostate cancer (PCa) has a high incidence worldwide. One of the major causes of PCa resistance is intratumoral hypoxia. In solid tumors, hypoxia is strongly associated with malignant progression and resistance to therapy, which is an indicator of poor prognosis. The antiproliferative effect and induced death caused by doxorubicin, epirubicin, cisplatin, and flutamide in a hormone-independent PCa cell line will be evaluated. The hypoxia effect on drug resistance to these drugs, as well as cell proliferation and migration, will be also analyzed. All drugs induced an antiproliferative effect and also cell death in the cell line under study. Hypoxia made the cells more resistant to all drugs. Moreover, our results reveal that long time cell exposure to hypoxia decreases cellular proliferation and migration. Hypoxia can influence cellular resistance, proliferation, and migration. This study shows that hypoxia may be a key factor in the regulation of PCa.
Highlights
Prostate cancer (PCa) is one of the most common diseases in the world, being the sixth leading cause of cancer death worldwide [1]
Pharmacological response of PC3 cell line to doxorubicin, epirubicin, cisplatin, and flutamide for incubation times of 24, 48, 72, and 96 h were shown at Figures 1(a), 1(b), 1(c), and 1(d)
Cell proliferation decreases with increasing drug concentration and incubation period, except for doxorubicin, epirubicin, and cisplatin at 96 h, in which there is a significant increase (P < 0.05) compared to 72 h (Table 2)
Summary
Prostate cancer (PCa) is one of the most common diseases in the world, being the sixth leading cause of cancer death worldwide [1]. Cancer cells have the capacity to adapt to hypoxic environments due to various genetic and epigenetic mechanisms and alterations at cellular level that contribute to adaptive changes which lead to a clinically aggressive phenotype, having hypoxic tumors a poor prognosis. These tumors are more difficult to treat, being highly resistant, presenting an increased risk of recurrence and progression [9, 10]. We aim at studying the antiproliferative effect and cell death induced by various agents of chemotherapy and hormonal therapy in a human hormone-independent PCa cell line Response to these treatment agents will be evaluated in normoxia and hypoxia conditions. Cellular proliferation and migration of the cell line under study will be determined under normoxia and hypoxia environments
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