Long non-coding RNA HNF1A-AS1 promotes cell proliferation and invasion via regulating miR-17-5p in non-small cell lung cancer.

Long non-coding RNA HNF1A-antisense 1 (lncRNA HNF1A-AS1) plays important roles in the progression of human tumors. The aim of this study is to unravel the underlying mechanism of HNF1A-AS1 in non-small cell lung cancer (NSCLC). In the present study, we found that HNF1A-AS1 was upregulation in NSCLC tissues and cell lines. High HNF1A-AS1 expression was associated with patients' advanced TNM stage and lymph node metastasis. Reduced HNF1A-AS1 expression inhibited lung cancer cells proliferation, invasion and increased cells apoptosis rate. Bioinformatics analysis and luciferase reporter assay revealed that HNF1A-AS1 interacted with miR-17-5p by directly targeting it. Rescue experiments showed that miR-17-5p suppression reversed the tumor-suppressing role of HNF1A-AS1 knockdown on NSCLC progression. Conclusion, our data indicated that lncRNA HNF1A-AS1 promoted lung cancer cells proliferation and invasion via regulating miR-17-5p, suggesting that HNF1A-AS1 could act as a potent therapeutic strategy for the treatment of NSCLC patients.

Zhang G ，An X ，Zhao H ，Zhang Q ，Zhao H ... -  《-》

lncRNA HNF1A-AS1 modulates non-small cell lung cancer progression by targeting miR-149-5p/Cdk6.

Growing evidence have shown the important regulation of lncRNAs (long noncoding RNAs) in non-small cell lung cancer (NSCLC). lncRNA hepatocyte nuclear factor 1 homeobox A (HNF1A)-antisense RNA 1 (AS1), an "oncogene", was reported to regulate human tumors progression. However, the molecular mechanism of HNF1A-AS1 involved in the development of NSCLC is still under investigation. In the current study, we found that HNF1A-AS1 was relatively upregulated in both NSCLC patient tissues and cell lines. Functional studies established that overexpression of HNF1A-AS1 promoted cell proliferation, cell cycle, invasion, and migration of NSCLC cells in vitro. The promotion abilities of HNF1A-AS1 on NSCLC cell progression were suppressed via knockdown of HNF1A-AS1. miR-149-5p was then proved to be a novel target of HNF1A-AS1, whose expression was negatively correlated with HNF1A-AS1 in NSCLC patient tissues and cell lines. HNF1A-AS1 increased the expression of cyclin-dependent kinase 6 (Cdk6) via sponging with miR-149-5p. Gain- and loss-of-functional studies indicated that HNF1A-AS1 promoted NSCLC progression partially through inhibition of miR-363-3p and induction of Cdk6. Subcutaneous xenotransplanted tumor model confirmed that interference of HNF1A-AS1 suppressed the tumorigenic ability of NSCLC via upregulation of miR-149-5p and downregulation of Cdk6 in vivo. In conclusion, our findings clarified the biologic significance of the HNF1A-AS1/miR-149-5p/Cdk6 axis in NSCLC progression and provided novel evidence that HNF1A-AS1 may be a new potential therapeutic target for the treatment of NSCLC.

Liu L ，Chen Y ，Li Q ，Duan P ... -  《-》

LncRNA NNT-AS1 promotes the proliferation, and invasion of lung cancer cells via regulating miR-129-5p expression.

Lung cancer is the leading cause of cancer related-deaths worldwide. Long non-coding RNAs (lncRNAs) are identified as important therapeutic targets in treatment of lung cancer. However, the roles of NNT-AS1 in lung cancer remain unclear. In the present study, we showed that the expression of NNT-AS1 was upregulated in non-small cell lung cancer (NSCLC) tissues and cell lines. High NNT-AS1 expression was associated with advanced tumor stage, and lymph node metastasis of NSCLC patients. In vitro function assays showed that NNT-AS1 inhibition could significantly reduce lung cancer cells proliferation and invasion ability. Then, we identified that NNT-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-129-5p in lung cancer. In addition, we showed that alteration in cell proliferation and invasion caused by NNT-AS1 downregulation could be rescued by miR-129-5p inhibitors. Thus, our study indicated that lncRNA NNT-AS1 exerted functions in NSCLC via altering NNT-AS1/miR-129-5p axis which provided a novel therapeutic target for lung cancer treatment.

Shen Q ，Jiang Y 《-》

E2F1-Induced Overexpression of Long Noncoding RNA SBF2-AS1 Promotes Non-Small-Cell Lung Cancer Metastasis Through Regulating miR-362-3p/GRB2 Axis.

Wang A ，Wang J 《-》

LncRNA NR2F2-AS1 promotes tumourigenesis through modulating BMI1 expression by targeting miR-320b in non-small cell lung cancer.

Recently, long noncoding RNAs (lncRNAs) are attracting wide attention in the field of cancer research because of its important role in cancer diagnosis and prognosis. But studies on the biological effects and relevant mechanisms of lncRNAs in non-small cell lung cancer (NSCLC) remain few and need to be enriched. Our study discussed the expression and biological effects of LncRNA NR2F2-AS1, and further explored its possible molecular mechanisms. As a result, elevated expression of NR2F2-AS1 was detected in NSCLC tissues and cells and was remarkably associated with the tumor, node, metastasis (TNM) stage and the status of lymphatic metastasis of patients. Down-regulated NR2F2-AS1 contributed to the promotion of cell apoptosis and the inhibition of cell proliferation and invasion in A549 and SPC-A-1 cells in vivo and vitro. Through bioinformatics analysis, NR2F2-AS1 functions as a ceRNA directly binding to miR-320b, BMI1 was a direct target of miR-320b. Combined with the following cellular experiments, the data showed that NR2F2-AS1 may influence the NSCLC cell proliferation, invasion and apoptosis through regulating miR-320b targeting BMI1.

Zhang S ，Zhang X ，Sun Q ，Zhuang C ，Li G ，Sun L ，Wang H ... -  《-》