Journal
CANCER COMMUNICATIONS
Volume 41, Issue 12, Pages 1275-1313Publisher
WILEY
DOI: 10.1002/cac2.12235
Keywords
colorectal; cancer stem cells; cell signaling; Wnt/beta-catenin pathway; Notch; Hedgehog; NF-kappa B; JAK/STAT signaling; PI3K/Akt/mTOR signaling; targeted therapy
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Funding
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES, Brazil)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq, Brazil)
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This review outlines strategies for eradicating CRC stem cells by modulating dysregulated pathways, with the aim of enhancing potential therapeutic schemes through the combination of conventional drugs and CSC-targeting drugs, leading to improved cure rates in anti-CRC therapy.
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 properties. 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 self-renewal properties, and most of them are dysregulated in CSCs, including the Wingless (Wnt)/beta-catenin, Notch, Hedgehog, nuclear factor kappa B (NF-kappa B), 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-beta (TGF-beta)/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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