Purpose: Non-small cell lung cancer (NSCLC) is a typical epithelial lung cancer with high metastasis, incidence and mortality. In recent years, long noncoding RNA small nucleolar RNA host gene 7 (SNHG7 ) has been identified as significant regulator in different cancer types, including NSCLC. However, the underlying molecular mechanism of SNHG7  during NSCLC tumorigenesis and progression remains largely unclear.
Methods: SNHG7  and miR-181a-5p expression in NSCLC tumors and cells were detected by qRT-PCR. Cell viability, migration, invasion and apoptosis were evaluated by CCK-8, transwell and flow cytometry assay, respectively. A549 and NCI-H1299 xenograft mice model was constructed by subcutaneously injecting cells stably transfected with sh-SNHG7 and sh-NC. The interaction between SNHG7  and miR-181a-5p was validated by luciferase reporter system, RIP and RNA pull down assay. Protein expression of cleaved caspase 3, proliferating cell nuclear antigen (PCNA), AKT, p-AKT, mammalian target of rapamycin (mTOR) and p-mTOR was analyzed by Western blot.
Results: SNHG7  expression was up-regulated while miR-181a-5p expression was down-regulated in NSCLC tumors, especially those from patients at Phase III+IV, compared with normal tissues. However, SNHG7  depletion attenuated tumor growth in vitro and in vivo. Moreover, miR-181a-5p inhibitor abolished SNHG7  silencing induced inhibition on proliferation, migration and invasion in NSCLC. Subsequently, we found SNHG7  modulated cell progression by targeting miR-181a-5p and activating AKT/mTOR signaling pathway.
Conclusion: SNHG7 accelerates proliferation, migration and invasion of NSCLC by suppressing miR-181a-5p through AKT/mTOR signaling pathway, thus presenting desirable biomarkers for NSCLC therapy.
Keywords: NSCLC, SNHG7, miR-181a-5p, AKT/mTOR pathway, progression