| Literature DB >> 33733384 |
Fernando Mendes1,2,3,4, Eurico Pereira5,6, Diana Martins7,5,8,6, Edgar Tavares-Silva5,8,6,9, Ana Salomé Pires5,8,6, Ana Margarida Abrantes5,8,6, Arnaldo Figueiredo5,8,6,9, Maria Filomena Botelho5,8,6.
Abstract
Bladder cancer (BC) is the most common cancer of the urinary tract and despite all innovations, remains a major challenge due to high morbidity and mortality. Genomic and epigenetic analyses allowed the discovery of new genes and pathways involved in the pathogenesis and regulation of BC. However, the effect on mortality has been modest and the development of new targets for BC treatment are needed. Recent evidence suggests that cancer cells are under increased stress associated with oncogenic transformation, with changes in metabolic activity and increased generation of reactive oxygen species (ROS). The increased amounts of ROS in cancer cells are associated with stimulation of cellular proliferation, promotion of mutations and genetic instability, as well as alterations in cellular sensitivity to anticancer agents. Since these mechanisms occur in cancer cells, there is a close link between oxidative stress (OS) and BC with implications in prevention, carcinogenesis, prognosis, and treatment. We address the role of OS as an enemy towards BC development, as well as an ally to fight against BC. This review promises to expand our treatment options for BC with OS-based therapies and launches this approach as an opportunity to improve our ability to select patients most likely to respond to personalized therapy.Entities:
Keywords: Antineoplastic drug resistance; Antioxidant activity; Carcinogenesis; Oxidative stress; Therapeutics; Urinary bladder neoplasms
Year: 2021 PMID: 33733384 DOI: 10.1007/s11033-021-06266-4
Source DB: PubMed Journal: Mol Biol Rep ISSN: 0301-4851 Impact factor: 2.316