癌变
生物
癌症研究
白藜芦醇
重编程
表观遗传学
癌症
癌细胞
癌症干细胞
上皮-间质转换
转移
细胞生物学
干细胞
细胞
遗传学
药理学
基因
作者
Aranka Brockmueller,Constanze Buhrmann,Amir Reza Moravejolahkami,Mehdi Shakibaei
标识
DOI:10.1016/j.jare.2024.01.005
摘要
Colorectal cancer (CRC), which is mainly caused by epigenetic and lifestyle factors, is very often associated with functional plasticity during its development. In addition, the malignant plasticity of CRC cells underscores one of their survival abilities to functionally adapt to specific stresses, including inflammation, that occur during carcinogenesis. This leads to the generation of various subsets of cancer cells with phenotypic diversity and promotes epithelial-mesenchymal transition (EMT), formation of cancer cell stem cell (CSC) and metabolic reprogramming. This can enhance cancer cell differentiation and facilitate tumorigenic potential, drug resistance and metastasis. The tumor protein p53 acts as one of the central suppressors of carcinogenesis by regulating its target genes, whose proteins are involved in the plasticity of cancer cells, autophagy, cell cycle, apoptosis, DNA repair. The aim of this review is to summarize the latest published research on resveratrol’s effect in the prevention of CRC, its regulatory actions, specifically on the p53 pathway, and its treatment options. Resveratrol, a naturally occurring polyphenol, is a potent inducer of a variety of tumor-controlling. However, the underlying mechanisms linking the p53 signaling pathway to the functional anti-plasticity effect of resveratrol in CRC are still poorly understood. Therefore, this review discusses novel relationships between anti-cellular plasticity/heterogeneity, pro-apoptosis and modulation of tumor protein p53 signaling in CRC oncogenesis, as one of the crucial mechanisms by which resveratrol prevents malignant phenotypic changes leading to cell migration and drug resistance, thus improving the ongoing treatment of CRC.
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