CircRNA G6PC3 promotes lung adenocarcinoma progression through enhancing HMGB1/Beclin 1 complex to induce autophagy.

[Display omitted] • Circ-G6PC3 is highly expressed in LUAD tissues and cells. • Circ-G6PC3 promotes cell proliferation and suppresses cell apoptosis in LUAD. • Circ-G6PC3 promotes LUAD cell proliferation through regulating autophagy. • Circ-G6PC3 could bind to HMGB1 and Beclin 1. • Circ-G6PC3 overexpression promotes the binding of HMGB1 with Beclin 1. Circular RNAs (circRNAs) have been corroborated to be vital modulators in multiple cancers, including lung adenocarcinoma (LUAD). Cellular autophagy is the way in which cells utilize lysosomes to degrade the damaged or senescent macromolecules and organelles through self-digestion. Reportedly, autophagy is closely associated with tumor progression. The current study targeted to probe circ-G6PC3 function in LUAD progression as well as its regulatory mechanism concerning autophagy. Through ISH, this research identified a high expression pattern of circ-G6PC3 in LUAD tissues compared to adjacent normal tissues. Consistently, high level of circ-G6PC3 was also determined in LUAD cells through quantitative real-time polymerase chain reaction (qRT-PCR). Through functional assays in vitro and in vivo , we found circ-G6PC3 augmentation promoted LUAD cell growth. Moreover, circ-G6PC3 facilitated LUAD cell proliferation via inducing autophagy. Mechanistically, circ-G6PC3 could bind with both HMGB1 and Beclin 1 and facilitate the binding between HMGB1 and Beclin 1, forming the circ-G6PC3-HMGB1-Beclin 1 complex. This study then ascertained that circ-G6PC3 boosted LUAD cell proliferation and suppressed the cell apoptosis through Beclin 1-mediated autophagy. In conclusion, circ-G6PC3 promotes LUAD progression through HMGB1-Beclin 1 complex-mediated autophagy. [ABSTRACT FROM AUTHOR]