Exploring the Effect of Gomisin A on Non‐Small Cell Lung Cancer With Network Pharmacology, Molecular Docking, In Vitro and In Vivo Assays

ABSTRACT Gomisin A is an active ingredient of Schisandra chinensis . Pre‐clinical studies suggest Gomisin A has good anti‐cancer activities against a variety of cancers, but its mechanism of action in non‐small cell lung cancer (NSCLC) is unclear. This study aims to explore the potential mechanism of Gomisin A in treating NSCLC. The SwissTargetPrediction, CTD, HERB and PharmMapper databases were used to collect related targets of Gomisin A. NSCLC‐related genes were obtained using the GEO, CTD, DisGeNET, OMIM, GeneCards, NCBI, and PharmGKB databases. The central targets and potential mechanisms of Gomisin A against NSCLC were screened using network pharmacology and molecular docking. Finally, the therapeutic activity of Gomisin A on NSCLC was verified by experiments. A total of 161 potential targets of Gomisin A against NSCLC were identified. TNF, AKT1, STAT3, and IL6 were identified as the central targets of Gomisin A. The binding energy of Gomisin A and the central targets was less than −5 kcal/mol. Gomisin A could inhibit NSCLC cell viability, migration and invasion and induce cell cycle arrest and apoptosis. Gomisin A also inhibited in vivo metastasis of NSCLC cells. In addition, Gomisin A could also reduce the expression level of the central targets and inhibit the PI3K‐Akt signaling pathway. In summary, Gomisin A may be a candidate drug for the treatment of NSCLC, and TNF, AKT1, STAT3, and IL6 are potential targets for Gomisin A in NSCLC treatment, and its therapeutic mechanism may be related to the PI3K‐Akt signaling pathway.