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Demao Li,1 Deshang Li,2 Linglei Meng,3 Juliang Liu,1 Chaokang Huang,4 Huijie Sun5 1Department of Thoracic Surgery, Xingtai People’s Hospital, Xingtai City, Hebei Province 054000, People’s Republic of China; 2Department of Clinical Laboratory, Xingtai People’s Hospital, Xingtai City, Hebei Province 054000, People’s Republic of China; 3Department of CT/MR, Xingtai People’s Hospital, Xingtai City, Hebei Province 054000, People’s Republic of China; 4Department of Pathology, Xingtai People’s Hospital, Xingtai City, Hebei Province 054000, People’s Republic of China; 5Department of Pharmacy, Xingtai Medical College, Xingtai City, Hebei Province 054000, People’s Republic of ChinaCorrespondence: Huijie SunDepartment of Pharmacy, Xingtai Medical College, West District, Xingtai City, Hebei Province 054000, People’s Republic of ChinaEmail ns6258@163.comBackground: 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 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.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.Keywords: ESCC, NLIPMT, survivin, miR-320, tumorigenesis