Cancer is a leading cause of death worldwide. Using network pharmacology and molecular docking techniques, this study aims to investigate the molecular mechanism of novel indole-quinoline derivative (SM7) in cancer by predicting a chain of hallmarks that can be targeted and subsequently inhibited to treat cancer with improved therapeutic effect. Out of total 25005 number of targets, 93 targets of SM7 were identified to be overlapped. David KEGG analysis retrieved 15 signaling pathways. Molecular docking of identified primary targets ie. STAT3, BCL2, ALB, MMP9 through protein-protein interaction analysis and compound-disease target-pathway, was performed. The results showed the significant affinity towards traced hub targets and complies with the data obtained from databases. Functional enrichment analysis also revealed the involvement of various important pathways which are related to cancer. In conclusion, SM7 may exert its anticancer effect by inhibiting the identified targets which are connecting links between various cell signaling pathways involved in cell survival and cancer progression. This study provides the theoretical groundwork for further in vitro and in vivo investigations of this molecule to develop it as anticancer agent.

The purpose of this study was to explore the anti-cancer activity and the possible mechanism of Dawa-ul kurkum (Duk) against diethylnitrosamine (DEN)-initiated hepatocarcinogenesis in male Wistar rats. We administered Duk at 3 doses, viz., 75, 150, and 300 mg/kg/day, 2 weeks before the DEN and continued it for 16 weeks. We found that Duk significantly reduced the DEN and 2-AAF induced phenotypical changes in rats and restored the activities of serum markers. Furthermore, Duk counteracted the oxidative stress induced by carcinogens as observed by restoration in the levels of superoxide dismutase (SOD) and catalase (CAT). Duk significantly diminished the levels of malondialdehyde (MDA) in a dose dependent manner and restored the liver microarchitecture as assessed by histopathological studies. The results of immunohistochemical staining showed that Duk inhibited the DEN-induced decrease in the number of cells positive for Bid and Caspase-9. It also reduces the number of cells positive for Cyclin D. This study shows that Duk significantly protects rat liver from hepatocarcinogenesis by regulating oxidative damage and restoring serum markers. The chemopreventive effect of Duk might be through induction of apoptosis.