自噬
内质网
基因沉默
细胞生物学
癌细胞
未折叠蛋白反应
机制(生物学)
生物
癌症
化学
癌症研究
基因
遗传学
细胞凋亡
认识论
哲学
作者
Sandhya Chipurupalli,Vincenzo Desiderio,Nirmal Robinson
出处
期刊:Methods in molecular biology
日期:2022-01-01
卷期号:: 211-220
被引量:1
标识
DOI:10.1007/978-1-0716-2513-2_16
摘要
The ability of the cancer cells to survive hostile environment depends on their cellular stressCancer cellcellular stress response mechanisms. These mechanisms also help them to develop resistance to chemotherapies. AutophagyAutophagy and more specifically organelle specific autophagy is one such adaptive mechanism that promotes drug resistance in cancer cells. Endoplasmic reticulum–specific autophagyAutophagyEndoplasmic reticulum–specific autophagy (ER-phagy) or ER-phagy has been more recently described to overcome ER-stress through the degradation of damaged ER. ER-resident proteins such as FAM134B act as ER-phagy receptors to specifically target damaged ER for degradation through autophagy. Moreover, we had recently deciphered that ER-phagy facilitates cancer cell survival during hypoxic stress and we predict that this process could play a critical role in the development of drug resistance in cancer cells. Therefore, here, we provide a lay description of how ER-phagy could be investigated biochemically by Western blot analysis and silencing ER-phagy receptor genes using small interfering RNAs (siRNA).
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