LncRNA NLIPMT Inhibits Tumorigenesis in Esophageal Squamous-Cell Carcinomas by Regulating miR-320/Survivin Axis

LncRNA NLIPMT 通过调节 miR-320/Survivin 轴抑制食管鳞状细胞癌的肿瘤发生

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作者:Demao Li, Deshang Li, Linglei Meng, Juliang Liu, Chaokang Huang, Huijie Sun

Background

LncRNA has been widely investigated for decades and plays critical roles in the progression of cancer. However, lncRNA NLIPMT, as a novel non-coding RNA, only was studied in breast cancer. This study aimed to explore the role of NLIPMT in esophageal squamous-cell carcinomas (ESCC). Materials and

Conclusion

We demonstrate that NLIPMT inhibits cell proliferation and migration and promotes cell cycle arrest and apoptosis in ESCC cells by regulating the miR-320/survivin axis. NLIPMT may be a novel prognosis biomarker in ESCC patients.

Methods

NLIPMT, miR320 and survivin mRNA in ESCC tissues (or non-tumor tissue) were detected by qRT-PCR. Dual-luciferase reporter assay was performed to assess the relationship between miR-320 and survivin. In ESCC cell lines KYSE510 and ECA109, miR-320 mimic and expression vectors carrying NLIPMT and survivin were used. Cell cycle, apoptosis, proliferation and migration were detected by flow cytometry, CCK-8, transwell assay, respectively. NIPMT, miR-320 and survivin expression were measured by qRT-PCR and Western blotting.

Results

NLIPMT was downregulated in ESCC and predicted poor survival of ESCC patients. NLIPMT was positively correlated with miR-320 and negatively correlated with survivin in ESCC tumor tissues. Dual-luciferase reporter assay showed that miR-320 directly regulated survivin. qRT-PCR and Western blotting showed that NLIPMT promoted miR-320 expression and inhibited survivin expression via up-regulating miR-320. Moreover, both NLIPMT and miR-320 overexpression inhibited cell proliferation and migration and promoted cell cycle arrest and apoptosis in ESCC cells, while their effects were abolished by survivin overexpression.

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