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https://www.arca.fiocruz.br/handle/icict/51052
EMERGING AGENTS THAT TARGET SIGNALING PATHWAYS TO ERADICATE COLORECTAL CANCER STEM CELLS
Author
Affilliation
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Hospital São Rafael. Rede D’Or/São Luiz. Salvador, Bahia, Brasil / Universidade do Estado da Bahia.Salvador, Bahia 41150-000, Brasil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Hospital São Rafael. Rede D’Or/São Luiz. Salvador, Bahia, Brasil / Universidade do Estado da Bahia.Salvador, Bahia 41150-000, Brasil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, Bahia, Brasil
Abstract
Colorectal cancer (CRC) represents the third most commonly diagnosed cancer and the second leading cause of cancer death worldwide. The modern concept of cancer biology indicates that cancer is formed of a small population of cells called cancer stem cells (CSCs), which present both pluripotency and self-renewal roperties. These cells are considered responsible for the progression of the disease, recurrence and tumor resistance. Interestingly, some cell signaling pathways participate in CRC survival, proliferation, and selfrenewal properties, and most of them are dysregulated in CSCs, including the Wingless (Wnt)/β-catenin, Notch, Hedgehog, nuclear factor kappa B (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), peroxisome proliferator-activated receptor (PPAR), phosphatidyl-inositol-3- kinase/Akt/mechanistic target of rapamycin (PI3K/Akt/mTOR), and transforming growth factor-β (TGF-β)/Smad pathways. In this review, we summarize
the strategies for eradicating CRC stem cells by modulating these dysregulated pathways, which will contribute to the study of potential therapeutic schemes, combining conventional drugs with CSC-targeting drugs, and allowing better cure rates in anti-CRC therapy.
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