Kang-Ai Injection Inhibits Gastric Cancer Cells Proliferation through IL-6/STAT3 Pathway

Area of Science:

• Oncology
• Pharmacology
• Molecular Biology

Background:

• Gastric cancer remains a significant global health challenge.
• Exploring novel therapeutic agents, including traditional Chinese medicines, is crucial for improving treatment outcomes.
• Understanding the molecular mechanisms of anti-cancer agents is essential for their effective clinical application.

Purpose of the Study:

• To elucidate the mechanisms by which Kang-Ai injection (KAI) inhibits gastric cancer cell proliferation.
• To investigate the role of the Interleukin-6/Signal Transducer and Activator of Transcription 3 (IL-6/STAT3) signaling pathway in KAI's anti-cancer effects.
• To determine the impact of KAI on cell cycle progression and apoptosis in gastric cancer cells.

Main Methods:

• Gastric cancer cell lines (MGC803, BGC823) were treated with varying concentrations of KAI.
• Cell proliferation was assessed using the MTT assay.
• Apoptosis and cell cycle distribution were analyzed by flow cytometry.
• Expression levels of IL-6, STAT3, and cell cycle-related proteins (cyclins, p21, RB) were quantified using qRT-PCR, ELISA, and Western blotting.

Main Results:

• KAI demonstrated dose- and time-dependent inhibition of gastric cancer cell proliferation.
• KAI treatment induced G1 phase arrest, characterized by increased p21 expression and decreased cyclin D1 and phosphorylated retinoblastoma (RB) protein levels.
• KAI significantly reduced IL-6 mRNA and protein expression, as well as STAT3 phosphorylation.
• Exogenous IL-6 partially reversed the anti-proliferative effects of KAI and restored STAT3 phosphorylation and cyclin D1 expression.

Conclusions:

• Kang-Ai injection (KAI) exerts anti-proliferative effects on gastric cancer cells.
• The mechanism involves the inhibition of the IL-6/STAT3 signaling pathway.
• KAI induces G1 phase arrest in gastric cancer cells, contributing to its anti-cancer activity.