SNHG7通过miR-181a-5p/E2F7轴促进非小细胞肺癌进展的机制研究

Abstract

Background Non-small-cell lung cancer (NSCLC) is a common malignant tumor with very high mortality. Small nucleolar RNA host gene 7 (SNHG7) was associated with many tumors progression. We aimed to explore the role and regulatory mechanism of SNHG7 in the development of NSCLC.Methods The expression of SNHG7, miR-181a-5p and E2F transcription factor 7 (E2F7) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of E2F7 was evaluated by Western blot. Cell Counting Kit-8 (CCK-8) assay was conducted to explore cell proliferation. Flow cytometry was used to examine cell apoptosis. The clonogenic examination was performed to reflect cell population dependence and proliferative ability. Transwell assay was used to assess cell migration and invasion. The potential target relationship between miR-181a-5p and SNHG7 or E2F7 was analyzed by dual-luciferase reporter assay. A xenograft mouse model was generated to verify the effect of SNHG7 on tumor growth in vivo.Results SNHG7 and E2F7 were increased, while miR-181a-5p was decreased in NSCLC. Knockdown of SNHG7 suppressed cell viability, clonogenic, migration, invasion and tumor growth, and promoted cell apoptosis. SNHG7 acted as a sponge of miR-181a-5p and E2F7 was directly interacted with miR-181a-5p. Overexpression of miR-181a-5p had the same functional effect as SNHG7 knockdown on the progression of NSCLC cells. E2F7 was negatively correlated with miR-181a-5p and positively correlated with SNHG7. Moreover, miR-181a-5p inhibition or E2F7 overexpression abolished the effect of SNHG7 knockdown on the progression of NSCLC cells.Conclusion SNHG7 regulated the development of NSCLC cells by the miR-181a-5p/E2F7 axis.