Highlights

1. The ER-Mt interactions are the important part of intracellular communication responsible for cell metabolism, development and death in the biological processes.

2. The ER-Mt regulations contribute to molecular mechanisms of diseases and vary among diseases, severities, stages and sensitivities to therapies.

3. The molecular signals during ER-Mt communication can be potential sources to discover and develop biology-, disease- and therapy-specific biomarkers and targets.

• A severe burn injury and its associated hypermetabolic response induces adipocyte dysfunction, fat catabolism, elevated fatty acids in the circulation and hepatic steatosis.
• Adipose triglyceride lipase (ATGL) plays a central role in adipose lipolysis and lipid metabolism.
• Targeting adipose-specific ATGL post-burn injury diminishes WAT browning, reduces fatty acids in the circulation and protects against liver dysfunction.

MLT regulated epigenetic modification of CES1 through SIRT1-mediated DNMT1 deacetylation. MLT-mediated CES1 expression induced lipid depletion, leading to ER stress-related apoptosis and blocking the intratumoral androgen synthesis that results in the inhibition of PCa progression and reversal of the enzalutamide resistance

Overexpression of HCN provides advantages for the survival and proliferation of cancer cells. The addition of Ivabradine blocks HCN channels and affects intracellular homeostasis of Ca²⁺. Subsequently, this induces ER-stress and triggers apoptosis. Also, it makes the cancer cells become more sensitive to other chemotherapeutic agents.

1. MSI2 expression was significantly upregulated in GBM, binding to SNORD12B and improving SNORD12B expression by increasing its stability.

2. SNORD12B regulated alternative polyadenylation process of transcriptional repressor ZBTB4 by competitively combining with FIP1L1.

3. ZBTB4 transcriptionally suppressed the expression of HK2, ACLY, and MSI2, forming a positive feedback regulatory loop to regulate the glycolipid metabolism and proliferation of GBM cell.

Tandem Mass Tags identified differentially expressed proteins (DEPs) between peritoneal metastasis (PM) and gastric cancer tissues, and showed that APOC2 was highly expressed in PM tissues.

APOC2 cooperates with CD36 to regulate EMT process via PI3K/AKT/mTOR signaling, which eventually promotes tumor progression and peritoneal metastasis in gastric cancer.