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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE327595 | GEO | 2026/04/15

REPOSITORIES: GEO

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Project description:Vascular Ehlers-Danlos syndrome (vEDS) is a severe connective tissue disorder caused by dominant mutations in the COL3A1 gene, which encodes type III collagen (COLLIII). COLLIII is primarily found in blood vessels and hollow organs, and its deficiency causes fragile soft connective tissues, with life-threatening arterial and organ ruptures. There are currently no targeted therapies available. Although disease results from COLLIII misfolding caused by triple helix structure disruption, the underlying pathomechanisms are largely unknown. To address this knowledge gap, we conducted a comprehensive transcriptome analysis using RNA-seq on a large cohort of dermal fibroblasts from vEDS patients and healthy donors. Our investigation revealed an intricate interplay between proteostasis abnormalities, inefficient endoplasmic reticulum (ER) stress response, and compromised autophagy, which may significantly impact the molecular pathology. We reported the first comprehensive map of complex gene expression networks, which may provide significant molecular insights into intricate interactions within cellular signaling pathways. the current RNA-seq data not only confirm these initial findings but also provide convincing evidence that ineffective proteostasis, unbalanced ER homeostasis, and compromised autophagy could substantially impact the molecular pathology driving the disease. aken together, or findings suggest that the accumulation of these misfolded aggregates can impair critical cellular functions such as ER proteostasis, adaptative responses to counteract ER stress (UPR and ERAD pathways), autophagy, mTOR pathway, and lysosome function. Perturbation of these key biological processes can have an impact on a range of cell activities, including differentiation, proliferation, and apoptosis, all of which are associated with the pathophysiology of vEDS. This work was supported by Fondazione Telethon and the “Associazione con Giacomo contro vEDS”, (Grant number: GSA21F001, Seed Grant Fall 2021 vEDS) to Nicola Chiarelli.

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

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