SNHG20 knockdown suppresses proliferation, migration and invasion, and promotes apoptosis in non-small cell lung cancer through acting as a miR-154 sponge.

Long noncoding RNAs (LncRNAs) play critical roles in the development and progression of cancers. However, little is known about the function and mechanism of lncRNAs in non-small cell lung cancer (NSCLC). In this study, we investigated the expression and functional role of lncRNA small nucleolar RNA host gene 20 (SNHG20) as well as its underlying mechanism in NSCLC. Our results showed that SNHG20 was significantly up-regulated in NSCLC tissues and cells. High SNHG20 expression was implicated with poor prognosis in NSCLC patients. Moreover, SNHG20 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NSCLC cells. Furthermore, SNHG20 could function as a competing endogenous RNA (ceRNA) to elevate ZEB2 and RUNX2 expression by sponging miR-154. Rescue assays revealed that miR-154 inhibition could reverse the inhibitory effect of SNHG20 silence on proliferation, migration and invasion in NSCLC cells. More importantly, SNHG20 knockdown suppressed tumor growth in NSCLC in vivo through suppressing miR-154 and elevating ZEB2 and RUNX2 expression. In summary, knockdown of lncRNA SNHG20 suppressed proliferation, migration and invasion, and promotes apoptosis through up-regulating ZEB2 and RUNX2 expression by sponging miR-154 in NSCLC, providing a promising therapeutic target for NSCLC patients.

Lingling J ，Xiangao J ，Guiqing H ，Jichan S ，Feifei S ，Haiyan Z ... -  《-》

Knockdown SNHG20 Suppresses Nonsmall Cell Lung Cancer Development by Repressing Proliferation, Migration and Invasion, and Inducing Apoptosis by Regulating miR-2467-3p/E2F3.

Chen H ，Tan X ，Ding Y 《-》

Knockdown of lncRNA DLX6-AS1 inhibits cell proliferation, migration and invasion while promotes apoptosis by downregulating PRR11 expression and upregulating miR-144 in non-small cell lung cancer.

Long non-coding RNA (lncRNA) distal-less homeobox 6 antisense 1 (DLX6-AS1) was reported to be dysregulated in lung cancer. However, detailed roles of DLX6-AS1 in the pathogenesis of non-small cell lung cancer (NSCLC) were largely unknown. The expression of DLX6-AS1 was measured in NSCLC tissues and cells by quantitative real-time PCR (qRT-PCR). The abundance of proline rich 11 (PRR11) were detected by qRT-PCR and western blot, respectively. The effects of DLX6-AS1 and PRR11 on cell proliferation, migration, invasion and apoptosis were explored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), transwell and flow cytometry analysis, respectively. Luciferase reporter assay, qRT-PCR and western blot were performed to confirm the interaction between miR-144 and DLX6-AS1 or PRR11. Tumor xenograft assay was performed to verify the role of DLX6-AS1 in NSCLC in vivo. DLX6-AS1 and PRR11 were elevated in NSCLC tissues and cells. DLX6-AS1 was positively correlated with PRR11 mRNA expression in NSCLC tissues. Knockdown of DLX6-AS1 and PRR11 significantly suppressed cell proliferation, migration and invasion and induced apoptosis in NSCLC cells, which was reversed by PRR11 overexpression. In addition, DLX6-AS1 and PRR11 were demonstrated to interact with microRNA-144 (miR-144) and DLX6-AS1 upregulated PRR11 expression by acting as a competing endogenous RNA (ceRNA) of miR-144 in NSCLC cells. Furthermore, DLX6-AS1 knockdown suppressed tumor growth in NSCLC in vivo by upregulating miR-144 and downregulating PRR11. Knockdown of DLX6-AS1 inhibited cell proliferation, migration, invasion and promoted apoptosis by downregulating PRR11 expression and upregulating miR-144 in NSCLC.

Huang Y ，Ni R ，Wang J ，Liu Y ... -  《-》

LncRNA SNHG16 promotes non-small cell lung cancer development through regulating EphA2 expression by sponging miR-520a-3p.

Recent evidence has found that lncRNA small nucleolar RNA host gene 16 (SNHG16) was associated with cell carcinogenesis in NSCLC. Here, we further investigated the precise functions and mechanisms of SNHG16 in NSCLC progression. The expression of SNHG16, microRNA (miR)-520a-3p and EPH Receptor A2 (EphA2) was measured using quantitative real-time polymerase chain reaction and western blot, respectively. Cell proliferation was determined using 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) assay. The migrated and invaded cells were measured by Transwell assay. Flow cytometry was used to detect apoptotic cells. The interaction between miR-520a-3p and SNHG16 or EphA2 was confirmed using a dual-luciferase reporter assay. We found that SNHG16 was upregulated in NSCLC tissues and cell lines, knockdown of SNHG16 inhibited cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. MiR-520a-3p directly bound to SNHG16 and miR-520a-3p, and SNHG16 acted as a ceRNA in regulating EphA2 through competitively binding to miR-520a-3p. Additionally, rescue assay exhibited the anticancer activity mediated by SNHG16 knockdown on NSCLC could be reversed by miR-520a-3p inhibition or EphA2 overexpression. SNHG16 promoted NSCLC development by regulating the miR-520a-3p/EphA2 axis, suggesting novel insights for the pathogenesis of NSCLC and new potential therapeutic targets for the treatment of NSCLC. Knockdown of SNHG16 inhibited NSCLC cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. SNHG16 directly interacted with miR-520a-3p. EphA2 was a target of miR-520a-3p. SNHG16 could regulate the expression of EphA2 by binding to miR-520a-3p. SNHG16 promoted NSCLC development by regulating the miR-520a-3p/EphA2 axis.

Yu L ，Chen D ，Song J 《-》

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》