期刊
CANCER COMMUNICATIONS
卷 41, 期 12, 页码 1275-1313出版社
WILEY
DOI: 10.1002/cac2.12235
关键词
colorectal; cancer stem cells; cell signaling; Wnt/beta-catenin pathway; Notch; Hedgehog; NF-kappa B; JAK/STAT signaling; PI3K/Akt/mTOR signaling; targeted therapy
类别
资金
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES, Brazil)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq, Brazil)
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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