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. 2021 Apr 30;12(5):424. doi: 10.1038/s41419-021-03715-7

Fig. 8. Schematic diagram of how MIR99AHG promotes autophagy and inhibits the progression of LUAD.

Fig. 8

In tumor cells, copy number deletion of 21q leads to the low expression of MIR99AHG and the miR-99a/let-7c/miR-125b2 cluster. MIR99AHG binds to ANXA2 to sustain cytoplasmic retention of ANXA2 which accelerates the biogenesis of ATG16L+ vesicles, and MIR99AHG-derived miR-99a targets mTOR, thus promoting autophagy and repressing the progression of LUAD. MIR99AHG/miR-99a-mediated autophagy enhanced the inhibition effect of these antitumor genes on the LUAD biogenesis, while loss of the autophagy promoted the tumor initiation induced by deficiency of these tumor suppressors.