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结直肠癌中的癌症干细胞:干性和治疗耐药性相关的信号通路。

Cancer stem cells in colorectal cancer: Signaling pathways involved in stemness and therapy resistance.

机构信息

Division of Genetics, Department of cell and molecular & microbiology, Faculty of Science and technology, University of Isfahan, Isfahan, Iran.

Department of chemistry and Biochemistry, South Dakota State University (SDSU), Brookings, SD, USA.

出版信息

Crit Rev Oncol Hematol. 2023 Feb;182:103920. doi: 10.1016/j.critrevonc.2023.103920. Epub 2023 Jan 23.


DOI:10.1016/j.critrevonc.2023.103920
PMID:36702423
Abstract

Colorectal cancer (CRC) is the third cause of cancer death worldwide. Although, in some cases, treatment can increase patient survival and reduce cancer recurrence, in many cases, tumors can develop resistance to therapy leading to recurrence. One of the main reasons for recurrence and therapy resistance is the presence of cancer stem cells (CSCs). CSCs possess a self-renewal ability, and their stemness properties lead to the avoidance of apoptosis, and allow a new clone of cancer cells to emerge. Numerous investigations inidicated the involvment of cellular signaling pathways in embryonic development, and growth, repair, and maintenance of tissue homeostasis, also participate in the generation and maintenance of stemness in colorectal CSCs. This review discusses the role of Wnt, NF-κB, PI3K/AKT/mTOR, Sonic hedgehog, and Notch signaling pathways in colorectal CSCs, and the possible modulating drugs that could be used in treatment for resistant CRC.

摘要

结直肠癌(CRC)是全球癌症死亡的第三大原因。尽管在某些情况下,治疗可以提高患者的生存率并降低癌症复发的风险,但在许多情况下,肿瘤可能会对治疗产生耐药性,从而导致复发。复发和耐药性的主要原因之一是存在癌症干细胞(CSC)。CSC 具有自我更新能力,其干细胞特性导致细胞避免凋亡,并允许新的癌细胞克隆出现。许多研究表明,细胞信号通路参与胚胎发育、组织稳态的生长、修复和维持,也参与结直肠 CSC 中干细胞特性的产生和维持。本文综述了 Wnt、NF-κB、PI3K/AKT/mTOR、Sonic hedgehog 和 Notch 信号通路在结直肠 CSC 中的作用,以及可能用于治疗耐药性 CRC 的调节药物。

相似文献

[1]
Cancer stem cells in colorectal cancer: Signaling pathways involved in stemness and therapy resistance.

Crit Rev Oncol Hematol. 2023-2

[2]
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Cancer Commun (Lond). 2021-12

[3]
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[4]
Dual-Blocking of PI3K and mTOR Improves Chemotherapeutic Effects on SW620 Human Colorectal Cancer Stem Cells by Inducing Differentiation.

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[5]
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Oncotarget. 2015-10-13

[6]
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[7]
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[8]
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[9]
Prostaglandin E2 Promotes Colorectal Cancer Stem Cell Expansion and Metastasis in Mice.

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[10]
Overexpression of PER3 Inhibits Self-Renewal Capability and Chemoresistance of Colorectal Cancer Stem-Like Cells via Inhibition of Notch and β-Catenin Signaling.

Oncol Res. 2017-5-24

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[2]
Stabilization of OLFML1 via mA Reader IGF2BP3 Drives CSC Characteristics Through Hedgehog Pathway Activation in CRC.

Int J Biol Sci. 2025-6-23

[3]
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Glob Med Genet. 2025-7-15

[4]
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[5]
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[7]
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