KK12, a novel anticancer peptide, induces apoptosis in human lung cancer A549 cells

Information from the abstract

Anticancer peptides (ACPs) have emerged as promising therapeutic agents owing to their potential for selective targeting of cancer cells. KK12 (amino acid sequence: KWWSKLKKFWKK) is a modified peptide derived from black soldier fly larvae; however, its anticancer potential and underlying mechanism of action remain unclear. This study evaluated the in vitro anticancer activity and mechanism of KK12 in human lung cancer A549 cells using an MTT assay to assess cytotoxicity, alongside Hoechst 33,342 staining and flow cytometry to evaluate morphological changes, cell cycle distribution, and apoptosis rates. Furthermore, the underlying molecular mechanisms were investigated using semi-quantitative RT-PCR and Western blot analysis. The results demonstrated that KK12 significantly inhibited A549 cell proliferation in a dose-dependent manner, with an IC50 value of 156 µM. Morphological and biochemical analyses revealed that KK12 induced apoptosis, as evidenced by nuclear condensation, sub-G1 accumulation indicative of apoptotic DNA fragmentation, and activation of apoptotic signaling pathways. Additionally, KK12 treatment increased BAX expression and promoted caspase-3 activation. Western blot and RT-PCR analyses further demonstrated dose-dependent modulation of BAX, cytochrome c, and caspase-3, suggesting the involvement of mitochondria-related apoptotic signaling. Collectively, these findings indicate that KK12 induces apoptotic cell death in A549 cells and provides a useful structural template for further engineering and optimization of peptide-based anticancer agents.

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