Sericin inhibits MDA-MB-468 cell proliferation via the PI3K/Akt pathway in triple-negative breast cancer

Triple negative breast cancer (TNBC) is a subtype of breast cancer characterized by an aggressive histology and poor prognosis, with limited treatment options in the clinic. In the present study, the effect of sericin, as an anti-cancer drug, on TNBC cell proliferation was investigated using a MTT assay, a colony formation assay and immunocytochemistry staining of Ki67. Results from the flow cytometry demonstrated that sericin induced G(0)/G(1) cell cycle arrest and promoted cellular apoptosis. Cell cycle and apoptosis-related proteins were detected via western blot analysis. Immunocytochemistry staining identified that P21 was translocated into the nucleus. Additionally, several pathways were significantly enriched in TNBC based on the Gene Expression Omnibus database, with the most prominent pathway being the PI3K/Akt signaling pathway. In TNBC MDA-MB-468 cells, sericin suppressed the PI3K/Akt pathway. All these findings suggested that sericin served a critical role in suppressing TNBC cell proliferation, inducing cell cycle arrest and promoting cellular apoptosis. The results indicated that the underlying molecular mechanism was, at least partially, via the downregulation of the PI3K/Akt signaling pathway.

Automated summary

The study found that sericin could effectively inhibit TNBC cell proliferation, induce cell cycle arrest, and promote cellular apoptosis, primarily by downregulating the PI3K/Akt signaling pathway.