Brazilin Inhibits the Proliferation of Non-Small Cell Lung Cancer by Regulating the STING/TBK1/IRF3 Pathway

Area of Science:

• Oncology
• Pharmacology
• Molecular Biology

Background:

• Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality globally.
• Brazilin, an isoflavonoid from Chinese herbs, shows anti-cancer effects but its NSCLC mechanism is unclear.

Purpose of the Study:

• To elucidate the anti-tumour mechanism of Brazilin in non-small cell lung cancer cells.
• To investigate Brazilin's effects on cell proliferation, apoptosis, cell cycle, and the STING pathway.

Main Methods:

• NSCLC cell lines were treated with Brazilin.
• Assessed cell proliferation, apoptosis, cell cycle distribution (G2 arrest), mitochondrial function, and ROS production.
• Investigated STING pathway activation, cytokine expression (CXCL10, CXCL9, CCL5), and effects of STING inhibition.

Main Results:

• Brazilin reduced NSCLC cell proliferation and induced apoptosis and G2 cell cycle arrest.
• Brazilin decreased Cyclin B1 and increased P21 expression, indicating cell cycle regulation.
• Brazilin triggered mitochondrial dysfunction, ROS production, and activated the STING pathway, upregulating CXCL10, CXCL9, and CCL5.
• STING pathway inhibition with H-151 increased cell viability, confirming STING's role in Brazilin-induced apoptosis.

Conclusions:

• Brazilin exhibits significant anti-NSCLC activity by inducing apoptosis and cell cycle arrest.
• The STING pathway is crucial for Brazilin's anti-tumour effects in NSCLC.
• Brazilin represents a promising therapeutic candidate for non-small cell lung cancer treatment.