GEO series

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

GSE327595 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/04/15 Platform GPL34284

Summary

Current studies have indicated an intricate and bidirectional regulatory interplay exists between autophagy and endoplasmic reticulum (ER) stress. 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. This feedback regulatory mechanism establishes the homeostasis between ER stress and autophagy by dynamically balancing stress responses and autophagic activities. Herein, we primarily examine the role of homeostasis between ER stress and autophagy throughout the functional gene transcription process in hepatocellular carcinoma cells.

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Also filed as BioProject PRJNA1451507 and SRA study SRP690792. Searching any of these in the dataset finder brings you back here.

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