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H. Li



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    MINI 34 - RNA and miRNA (ID 162)

    • Event: WCLC 2015
    • Type: Mini Oral
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      MINI34.09 - The Long Non-Coding RNA AK126698 Modulates Wnt/β-Catenin Signaling Through FZD-8 Silencing in Non-Small-Cell Lung Cancer (ID 737)

      19:15 - 19:20  |  Author(s): H. Li

      • Abstract

      Background:
      Recent evidence indicates that long non-coding RNAs (lncRNAs) play a critical role in the regulation of cellular processes, such as differentiation, proliferation and metastasis. These lncRNAs are found to be dysregulated in a variety of cancers. In our previous study, we have demonstrated that lncRNA AK126698 regulated A549 cells cisplatin resistance partly through Wnt/β-catenin signaling. However, the clinical significance of lncRNA AK126698, and its’ molecular mechanisms of controlling cancer cell proliferation and migration are still unclear.

      Methods:
      Expression of lncRNA AK126698 was analyzed in 55 non-small cell lung cancer (NSCLC) tissues and 3 NSCLC cell lines using quantitative polymerase chain reaction (qPCR) assays. Gain and loss of function approaches were used to investigate the biological role of AK126698 in NSCLC cells. The effects of AK126698 on cell proliferation were evaluated by CCK-8 and colony formation assays. Apoptosis was evaluated by flow cytometry. Protein levels of AK126698 targets were determined by western blotting and fluorescent immunohistochemistry.

      Results:
      AK126698 expression was significantly decreased in NSCLC tumor tissues compared with normal lung tissues. Additionally, reduced AK126698 expression was associated with larger tumor size and advanced pathological staging of NSCLC patients. Ectopic expression of AK126698 impaired cell proliferation and migration and induced apoptosis in vitro. However, knockdown of AK126698 expression promoted cell migration and invasionin in vitro. In addition, the expression of FZD8 was inversely correlated with AK126698 in both NSCLC tissues and cell lines and that over-expression of AK126698 could significantly down-regulate the expression of gene downstream of FZD8, including β-catenin, CyclinD1 and c-Myc.

      Conclusion:
      The results of present study indicate that lncRNA AK126698 might serve as a suppressor that regulates the pathogenesis of NSCLC through Wnt/β-catenin signaling pathway. It may provide a new target for therapeutic intervention of NSCLC.