The homeostasis of endoplasmic reticulum stress and autophagy regulates functional gene transcription in hepatocellular carcinoma cells

Both processes collaborate to maintain cellular homeostasis and play critical roles in the development and progression of hepatocellular carcinoma. On one hand, autophagy alleviates ER stress by degrading misfolded proteins, acting as a complementary mechanism to the unfolded protein response (UPR) for restoring ER homeostasis.

It can also directly mitigate ER stress by removing specific stressors. On the other hand, ER stress is capable of activating numerous associated functional proteins of autophagy. Upon activation, autophagy decreases the level of ER stress via multiple pathways.