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W. Chenchen

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    Poster Display session (Friday) (ID 65)

    • Event: ELCC 2018
    • Type: Poster Display session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
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      18P - The pseudogene DUXAP10 promotes an aggressive phenotype through binding with LSD1 and repressing LATS2 and RRAD in non-small cell lung cancer (ID 497)

      12:30 - 13:00  |  Presenting Author(s): W. Chenchen

      • Abstract

      Pseudogenes have been considered as non-functional transcriptional relics of human genomic for long time. However, recent studies revealed that they play a plethora of roles in diverse physiological and pathological processes, especially in cancer, and many pseudogenes are transcribed into long noncoding RNAs and emerging as a novel class of lncRNAs. However, the biological roles and underlying mechanism of pseudogenes in the pathogenesis of non-small cell lung cancer are still incompletely elucidated.

      Real-time polymerase chain reaction (PCR) was used to examine DUXAP10 expression in NSCLC cell lines/tissues compared with normal epithelial cells/adjacent non-tumorous tissues. Cox proportional hazards regression models were performed to further confirm the prognostic role of DUXAP10. Cell proliferation assays were performed to detect the biological effects of DUXAP10 in gastric cancer cells. Real-time PCR, western-blot and immunohistochemistry were used to evaluate the mRNA and protein expression of LATS2 and RRAD.

      This study identifies a putative oncogenic pseudogene DUXAP10 in NSCLC, which is located in 14q11.2 and 2398 nt in length. Firstly, we found that DUXAP10 was significantly up-regulated in 93 human NSCLC tissues and cell lines, and increased DUXAP10 was associated with patients’ poorer prognosis and short survival time. Furthermore, the loss and gain of functional studies including growth curves, migration, invasion assays and in vivo studies verify the oncogenic roles of DUXAP10 in NSCLC. Finally, the mechanistic experiments indicate that DUXAP10 could interact with Histone demethylase Lysine specific demethylase1 (LSD1) and repress tumor suppressors Large tumor suppressor 2 (LATS2) and Ras-related associated with diabetes (RRAD) transcription in NSCLC cells.

      These findings demonstrate DUXAP10 exerts the oncogenic roles through binding with LSD1 and epigenetic silencing LATS2 and RRAD expression. Our investigation reveals the novel roles of pseudogene in NSCLC, which may serve as new target for NSCLC diagnosis and therapy.

      Clinical trial identification:

      Legal entity responsible for the study:
      The Second Affiliated Hospital of Nanjing Medical University

      National Natural Science Foundation of China (No. 81472198), the Key Clinical Medicine Technology Foundation of Jiangsu Province (No BL2014096), the Medical Innovation Team Foundation of the Jiangsu Provincial Enhancement Health Project (No.21), “333 high class Talented Man Project” (No. BRA2016509)

      All authors have declared no conflicts of interest.