Regulation of inflammatory response by LINC00346 via miR-25-3p-mediated modulation of the PTEN/PI3K/AKT/NF-κB pathway

Area of Science:

• Molecular Biology
• Cell Biology
• Immunology

Background:

• Long intergenic non-coding RNA 346 (LINC00346) is implicated in atherosclerosis and cancer.
• The role of LINC00346 in inflammation remains largely uncharacterized.
• Understanding LINC00346's function in inflammatory pathways is crucial.

Purpose of the Study:

• To investigate the expression pattern and function of LINC00346 in human macrophages.
• To elucidate the molecular mechanism underlying LINC00346's role in inflammation.
• To explore the relationship between LINC00346, PTEN, and NF-κB signaling.

Main Methods:

• THP-1 cells were treated with lipopolysaccharide (LPS) to induce inflammation.
• LINC00346 expression was modulated (overexpression/knockdown).
• Dual luciferase assays and decoy RNAs were used to identify RNA-RNA interactions; PTEN, PI3K, AKT, and NF-κB pathways were analyzed.

Main Results:

• LPS induced LINC00346 expression in THP-1 cells.
• LINC00346 modulated LPS-induced NF-κB activation and pro-inflammatory cytokine production.
• LINC00346 acts as a miR-25-3p sponge, enhancing PTEN expression, which inhibits the PI3K/AKT/NF-κB pathway.

Conclusions:

• LINC00346 plays a significant role in regulating inflammatory responses in macrophages.
• The LINC00346/miR-25-3p/PTEN axis is a key regulator of the PI3K/AKT/NF-κB pathway.
• This finding provides novel insights into the molecular mechanisms of inflammation and potential therapeutic targets.