miR-193b availability is antagonized by LncRNA-SNHG7 for FAIM2-induced tumour progression in non-small cell lung cancer

Kelin She, Hui Yan, Jun Huang, Huaping Zhou, Jianxing He
Cell Proliferation 2018, 51 (1)

OBJECTIVES: Long non-coding RNAs have identified to involve into the tumour cell proliferation, apoptosis and metastasis. We previously found that up-regulated LncRNA-SNHG7 (SNHG7) positively correlated to the Fas apoptosis inhibitory molecule 2 (FAIM2) in lung cancer cells with unclear mechanism.

METHODS: Non-small cell lung cancer (NSCLC) and relative normal tissues (n = 25) were collected. The SNHG7 expression and function in NSCLC was determined. The SNHG7-miR 193b-FAIM2 network was analysed in vitro and vivo.

RESULTS: We reported that oncogene SNHG7 predicted a poor clinical outcome and functioned as competitive endogenous RNA (ceRNA) antagonized microRNA-193b (miR-193b) to up-regulate the FAIM2 level in NSCLC. Bioinformatic analysis predicted that SNHG7 harboured miR-193b-binding sites, and we found decreased miR-193b levels in NSCLC tissues when compared to relative normal tissues. Luciferase assays indicated that overexpression of miR-193b inhibited the Ruc expression of plasmid with miR-193b-binding sites of SNHG7 in a dose-dependent manner. Ectopically expressed SNHG7 also as a molecular sponge sequestered endogenous miR-193b. Besides, FAIM2 was found to be directly targeted by miR-193b. The restoration of miR-193b levels in NSCLC cell lines A549 and H125 suppressed the expression of FAIM2 and related tumour proliferation, metastasis and induced apoptosis. However, forced expression of SNHG7 could down-regulate miR-193b to elevate the FAIM2 level of tumour cells, leading to impaired miR-193b/FAIM2-induced tumour progression. Knockdown of SNHG7 in vivo significantly delayed the tumour growth with decreased tumour volume, which accompanied with enhanced miR-193b expression and reduced FAIM2 levels.

CONCLUSION: The results indicated that miR-193b is indispensible for the ceRNA role of SNHG7 in FAIM2-supported tumourigenesis of lung cancer.

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