LINC00852 participates in the phycocyanin-mediated restrained vitality of non-small cell lung cancer cells via miR-29a-3p/LAMTOR1 axis

Abstract

Phycocyanin has been reported to exert antineoplastic function in non-small cell lung cancer (NSCLC), while the underlying molecular mechanism is still largely unclear. In this study, a whole transcriptome resequencing was employed. Results showed that lncRNA LINC00852 was inhibited by phycocyanin in NSCLC cells. Knockdown LINC00852 expression resulted in the attenuated proliferation, viability and migration ability of NSCLC cells. Meanwhile, dual-luciferase reporter assay indicated that LINC00852 acted as a ceRNA of miR-29a-3p which further targets regulator complex protein LAMTOR1 (LAMTOR1). Overexpression miR-29a-3p or knockdown LAMTOR1 expression decreased the activity of NSCLC cells, respectively. Moreover, AMPK signaling was activated upon LINC00852 knockdown, miR-29a-3p enhancement or LAMTOR1 inhibition, which was in consistent with the phycocyanin exposure results. In summary, we demonstrated that LINC00852 played a key role in phycocyanin-mediated NSCLC regulation process, and the epigenetic signaling LINC00852/miR-29a-3p/LAMTOR1 may be considered as novel molecular targets for fighting NSCLC base on marine functional foods.

Keywords

• Phycocyanin
• LINC00852/miR29a-3p/LAMTOR1 axis
• NSCLC
• Cell activity
• AMPK pathway