Analysis of ER-Phagy in Cancer Drug Resistance
Sandhya Chipurupalli1,2, Vincenzo Desiderio3, Nirmal Robinson4
1Cellular Stress and Immune Response Laboratory, Centre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Abstract:
The ability of the cancer cells to survive hostile environment depends on their cellular stress response mechanisms. These mechanisms also help them to develop resistance to chemotherapies. Autophagy and more specifically organelle specific autophagy is one such adaptive mechanism that promotes drug resistance in cancer cells. Endoplasmic reticulum-specific autophagy 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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