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CD133 干细胞标志物与结直肠癌中自噬和细胞凋亡的关联

Interconnection of CD133 Stem Cell Marker with Autophagy and Apoptosis in Colorectal Cancer.

机构信息

Immunology Division, Department of Internal Medicine and Hematology, Semmelweis University, 1088 Budapest, Hungary.

出版信息

Int J Mol Sci. 2024 Oct 18;25(20):11201. doi: 10.3390/ijms252011201.

DOI:10.3390/ijms252011201
PMID:39456981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11508732/
Abstract

CD133 protein expression is observable in differentiated cells, stem cells, and progenitor cells within normal tissues, as well as in tumor tissues, including colorectal cancer cells. The CD133 protein is the predominant cell surface marker utilized to detect cancer cells exhibiting stem cell-like characteristics. CD133 alters common abnormal processes in colorectal cancer, such as the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) and Wnt/β-catenin pathways. Autophagy is a cellular self-digestion mechanism that preserves the intracellular milieu and plays a dual regulatory role in cancer. In cancer cells, apoptosis is a critical cell death mechanism that can impede cancer progression. CD133 can modulate autophagy and apoptosis in colorectal cancer cells via several signaling pathways; hence, it is involved in the regulation of these intricate processes. This can be an explanation for why CD133 expression is associated with enhanced cellular self-renewal, migration, invasion, and survival under stress conditions in colorectal cancer. The purpose of this review article is to explain the complex relationship between the CD133 protein, apoptosis, and autophagy. We also want to highlight the possible ways that CD133-mediated autophagy may affect the apoptosis of colorectal cancer cells. Targeting the aforementioned mechanisms may have a significant therapeutic role in eliminating CD133-positive stem cell-phenotype colorectal cancer cells, which can be responsible for tumor recurrence.

摘要

CD133 蛋白在正常组织和肿瘤组织中的分化细胞、干细胞和祖细胞中都有表达,包括结直肠癌细胞。CD133 蛋白是用于检测具有干细胞样特征的癌细胞的主要细胞表面标志物。CD133 改变了结直肠癌的常见异常过程,如磷酸肌醇 3-激酶(PI3K)/蛋白激酶 B(AKT)和 Wnt/β-连环蛋白途径。自噬是一种细胞自我消化的机制,可维持细胞内环境,并在癌症中发挥双重调节作用。在癌细胞中,细胞凋亡是一种关键的细胞死亡机制,可以阻碍癌症的进展。CD133 可以通过几种信号通路调节结直肠癌细胞中的自噬和细胞凋亡;因此,它参与了这些复杂过程的调节。这可以解释为什么 CD133 表达与结直肠癌细胞中增强的细胞自我更新、迁移、侵袭和应激条件下的存活有关。本文综述的目的是解释 CD133 蛋白、细胞凋亡和自噬之间的复杂关系。我们还想强调 CD133 介导的自噬可能影响结直肠癌细胞凋亡的可能途径。针对上述机制可能在消除 CD133 阳性的干细胞表型结直肠癌细胞方面具有重要的治疗作用,这些细胞可能是肿瘤复发的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b339/11508732/dc591da7eab7/ijms-25-11201-g005.jpg
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