Phycocyanin diminishes the viability of non-small cell lung cancer cells via induction of autophagy.

[Display omitted] • Phycocyanin inhibits the growth of NSCLC cells. • Phycocyanin induces autophagy and autophagy flux in NSCLC cells. • AMPK signaling pathway activation is involved in phycocyanin-treated lung cancer cells. • Phycocyanin attenuated viability of multiple lung cancer cells through promoting autophagy. Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality worldwide. Phycocyanin, a type of marine food additives, has been reported to exert antineoplastic effects in NSCLC. The aim of this study was to investigate roles of autophagy in the anticancer process of phycocyanin in NSCLC. Results showed that phycocyanin increased LC3-II/LC3-I ratio and decreased p62 level of NSCLC cells in a dose- and time-dependent manner. Laser scanning confocal observation of autophagic LC3 puncta showed phycocyanin promotes autophagy flux of NSCLC cells. In addition, AMPK signaling was activated upon phycocyanin treatment. Strikingly, phycocyanin was shown to synergistically affect the autophagy of cells with rapamycin and chloroquine, thus concertedly inhibiting the viabilities of NSCLC cells. These results indicated that the antineoplastic effect of phycocyanin could be attributed to the activated autophagy and AMPK signaling pathway. Thus, targeting autophagy could be a promising way to improve NSCLC though phycocyanin. [ABSTRACT FROM AUTHOR]