Journal
CELLS
Volume 9, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/cells9081850
Keywords
bladder cancer; DNA methylation; DNA methyltransferases; nucleoside analogues; therapy
Categories
Funding
- European Regional Development Fund (FEDER) grants from Science and Innovation [SAF2015-66015-R, PID2019-110758RB-I00]
- Instituto de Salud Carlos III (RETIC) [RD12/0036/0009]
- Instituto de Salud Carlos III (CIBERONC) [CB16/12/00228]
- FCT Fundacao para a Ciencia e Tecnologia grant [SFRH/BD/144241/2019]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/144241/2019] Funding Source: FCT
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Bladder cancer (BC) is the tenth most frequent cancer worldwide and is associated with high mortality when diagnosed in its most aggressive form, which is not reverted by the current treatment options. Thus, the development of new therapeutic strategies, either alternative or complementary to the current ones, is of major importance. The disruption of normal epigenetic mechanisms, namely, DNA methylation, is a known early event in cancer development. Consequently, DNA methyltransferase (DNMT) inhibitors constitute a promising therapeutic target for the treatment of BC. Although these inhibitors, mainly nucleoside analogues such as 5-azacytidine (5-aza) and decitabine (DAC), cause re-expression of tumor suppressor genes, inhibition of tumor cell growth, and increased apoptosis in BC experimental models and clinical trials, they also show important drawbacks that prevent their use as a valuable option for the treatment of BC. However, their combination with chemotherapy and/or immune-checkpoint inhibitors could aid in their implementation in the clinical practice. Here, we provide a comprehensive review of the studies exploring the effects of DNA methylation inhibition using DNMTs inhibitors in BC, from in vitro and in vivo studies to clinical trials.
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