SNHG11 contributes to NSCLC cell growth and migration by targeting miR-485-5p/BSG axis.

Accumulating studies implied that long noncoding RNAs (lncRNAs) act as essential factors in regulating diverse biological behaviors of cancers. Small nucleolar RNA host gene 11 (SNHG11) has been reported as for its oncogenic properties in several cancer types. However, it is unclear whether SNHG11 exerts functions in non-small cell lung cancer (NSCLC) remains unclear. The aim of this study was to inspect the role and regulatory mechanism of SNHG11 in NSCLC. The expression of SNHG11 in NSCLC cells was analyzed by qRT-PCR. Functional experiments were carried out to determine the effects of SNHG11 silence on the biological behaviors of NSCLC cells, including growth, migration and epithelial-mesenchymal transition. The inhibition of above functions was observed after SNHG11 was silenced. Subcellular fractionation and FISH assays were performed to detect the cellular distribution of SNHG11. Moreover, SNHG11 was found to be a sponge of miR-485-5p that could directly target to Basigin (BSG) mRNA. The interaction between SNHG11 and miR-485-5p as well as between miR-485-5p and BSG was proven by RNA pull down and luciferase reporter assays. Restoration assay confirmed the involvement of miR-485-5p and BSG in SNHG11-mediated NSCLC cellular functions. Conclusively, SNHG11 was overexpressed in NSCLC and functioned as a miR-485-5p sponge to up-regulate BSG.

Cheng R ，Lu X ，Xu C ，Zhang F ，Zhang G ... -  《-》

Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p.

Lu W ，Zhang H ，Niu Y ，Wu Y ，Sun W ，Li H ，Kong J ，Ding K ，Shen HM ，Wu H ，Xia D ，Wu Y ... -  《Molecular Cancer》

Long non-coding RNA PRNCR1 modulates non-small cell lung cancer cell proliferation, apoptosis, migration, invasion, and EMT through PRNCR1/miR-126-5p/MTDH axis.

Non-small cell lung cancer (NSCLC) is a highly malignant tumor. Accumulating evidence suggested that prostate cancer non-coding RNA 1 (PRNCR1) participated in the pathogenesis of NSCLC, whereas the elaborate mechanism remains unclear. Hence, the role of PRNCR1 in the progression of NSCLC was investigated. Levels of PRNCR1, microRNA-126-5p (miR-126-5p), and metadherin (MTDH) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was measured using Cell Counting Kit-8 (CCK-8). Flow cytometry was conducted to determine cell apoptosis. Besides, transwell assay was performed to detect cell migration and invasion in NSCLC cells. The expression levels of E-cadherin, N-cadherin, Vimentin, and MTDH were detected via Western blot. Dual-luciferase reporter, RNA immunoprecipitation, and RNA pull down assays were employed to verify the relationship between miR-126-5p and PRNCR1 or MTDH. PRNCR1 and MTDH levels were highly expressed, while miR-126-5p expression was lowly expressed in NSCLC tissues and cell lines. Knockdown of PRNCR1 promoted cell apoptosis, impeded proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in NSCLC cells, and these effects were abrogated by its target gene of miR-126-5p inhibitor. Moreover, MTDH as the target of PRNCR1, its overexpression reversed the impacts of miR-126-5p mimic on cell behaviors and EMT in vitro. Finally, PRNCR1 and miR-126-5p regulated MTDH expression. PRNCR1 modified cell behaviors and EMT via miR-126-5p/MTDH axis in NSCLC cells, providing a novel thinking for clinical treatment of NSCLC.

Guo R ，Hu T ，Liu Y ，He Y ，Cao Y ... -  《-》

Long non-coding RNA SNHG11 promotes cell proliferation, invasion and migration in glioma by targeting miR-154-5p.

Geng YB ，Xu C ，Wang Y ，Zhang LW ... -  《-》

LncRNA MALAT1 accelerates non-small cell lung cancer progression via regulating miR-185-5p/MDM4 axis.

Non-small cell lung cancer (NSCLC) is the commonest malignancy with high death rate around the world. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is greatly overexpressed in multifarious cancers, including NSCLC. However, the precise mechanism of MALAT1 in NSCLC tumorigenesis is blurry. This paper aims to investigate the theory of MALAT1 action in NSCLC progression. The levels of MALAT1, microRNA (miR)-185-5p, and mouse double minute 4 protein (MDM4) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation and apoptosis were, respectively, determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and flow cytometry. Cell migratory and invasive abilities were inspected by transwell assay. The binding relationship between miR-185-5p and MALAT1 or MDM4 was confirmed by dual-luciferase reporter assay. The impacts of MALAT1 on tumor growth in vivo were measured by a xenograft experiment. We found MALAT1 and MDM4 were upregulated and MALAT1 positively regulated the MDM4 expression. MALAT1 and MDM4 deletion significantly hindered the proliferation, metastasis, and expedited the apoptosis of NSCLC cells. MDM4 overexpression partly overturned the influence of MALAT1 downregulation on cell development. Moreover, miR-185-5p, as a target of MALAT1, could directly target MDM4, and miR-185-5p upregulation exerted inhibitory effects on NSCLC cells. Besides, knockdown of MALAT1 inhibited tumor growth in vivo through miR-185-5p/MDM4 axis in NSCLC. Collectively, MALAT1 contributed to proliferation, migration, invasion, and impeded apoptosis by regulating the MDM4 expression mediated by miR-185-5p in NSCLC cells.

Wang D ，Zhang S ，Zhao M ，Chen F ... -  《Cancer Medicine》