The Second Affiliated Hospital, Medical College, Xi’an Jiaotong University, Xi’an, China
Copyright 2016, American College of Chest Physicians. All Rights Reserved.
SESSION TITLE: Lung Cancer II
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM
PURPOSE: This study aimed to screen NSCLC metastasis associated lncRNAs and explore the effects and mechanisms of objective lncRNA in NSCLC metastasis.
METHODS: LncRNA chip technology was employed to screen the differentially expressed lncRNAs between high metastatic cell line 95D and low metastatic cell line 95C. A stable 95D cell line that silenced the expression of objective lncRNA was constructed using lentiviral interference technology. MTT, transwell assay, adhesion assay and electron microscopy were used to detect changes in cell proliferation, migration, invasion, adhesion ability and cell shape. QPCR, flow cytometry, Zymogram Gels and Western blot identified NSCLC metastasis related genes and proteins. Using the nude mice model, size of the primary tumor was recorded and expressions of proteins were evaluated.
RESULTS: 313 lncRNAs were screened and LncRNA RP11-366L20.3 was found to promote NSCLC metastasis. The expression of lncRNA RP11-366L20.3 was inversely associated with E-cadherin and nm23-H1 levels (p<0.05), and positively associated with C-erbB-2 and Ezrin expression (p<0.05) in 95D cell in vitro. LncRNA RP11-366L20.3 may promote metastasis in 95D cell in vitro through Wnt/β-catenin signaling pathway. LncRNA RP11-366L20.3 promoted tumor growth in vivo.
CONCLUSIONS: LncRNA RP11-366L20.3 holds potential as the target for gene therapy of NSCLC metastasis.
CLINICAL IMPLICATIONS: It provides a new experimental basis for the treatment of lung cancer.
DISCLOSURE: The following authors have nothing to disclose: Shuanying Yang, Yujie Zhong, Xuemei Zhang, Wei Li, Zongjuan Ming, Yuping Zhang, Wenjing Deng, Hongyang Shi, Na Fan, Zequn Niu, Xia Meng, Zongfang Li, Chen Huang
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