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Role of the ER-induced UPR pathway, apoptosis, and autophagy in colorectal cancer

未折叠蛋白反应 内质网 自噬 程序性细胞死亡 细胞凋亡 细胞生物学 细胞质 细胞 信号转导 癌症研究 生物 生物化学
作者
Elmira Aboutalebi Vand Beilankouhi,Mir Amirhossein Sajadi,Iraj Alipourfard,Peyman Hassani,Mohammad Valilo,Reza Safaralizadeh
出处
期刊:Pathology Research and Practice [Elsevier]
卷期号:248: 154706-154706 被引量:9
标识
DOI:10.1016/j.prp.2023.154706
摘要

When large amounts of misfolded or unfolded proteins accumulate in the endoplasmic reticulum (ER) in response to stress, a process called unfolded protein response (UPR) is activated. The disruption of this process leads to many diseases including diabetes, neurodegenerative diseases, and many cancers. In the process of UPR in response to stress and unfolded proteins, specific signaling pathways are induced in the endoplasmic reticulum and subsequently transmitted to the nucleus and cytoplasm, causing homeostasis and restoring the cell's normal condition with reducing protein translation and synthesis. The UPR response followed by stress enhancement balances cell survival with death, therefore in this condition cells decide either to survive or have the path of apoptosis ahead. However, in some cases, this balance is disturbed and the UPR pathway is chronically activated or not activated and the cell conditions lead to cancer. This study aimed to briefly investigate the association between ER stress, UPR, apoptosis, and autophagy in colorectal cancer (CRC). Moreover, in current study, we will try to demonstrate canonical ways and methods for the treatment of CRC cells with attenuated ER stress.
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