SNHG7 Contributes to the Progression of Non-Small-Cell Lung Cancer via the SNHG7/miR-181a-5p/E2F7 Axis
Authors Wang L, Zhang L, Wang L
Received 3 December 2019
Accepted for publication 16 April 2020
Published 7 May 2020 Volume 2020:12 Pages 3211—3222
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Eileen O'Reilly
Liming Wang,1 Lili Zhang,2 Liwei Wang3
1Department of Interventional, Shandong Provincial Chest Hospital, Jinan, Shandong, People’s Republic of China; 2Thoracoscopic Ward, Shandong Provincial Chest Hospital, Jinan, Shandong, People’s Republic of China; 3Department of Radiology, Tianbao Township Health Center, Taian, Shandong, People’s Republic of China
Correspondence: Liwei Wang
Department of Radiology, Tianbao Township Health Center, Tianbao Town, High-Tech Zone, Taian City, Shandong Province, People’s Republic of China
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.
Keywords: SNHG7, miR-181a-5p, E2F7, NSCLC
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