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Y. Lou



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    P2.01 - Poster Session with Presenters Present (ID 461)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Biology/Pathology
    • Presentations: 1
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      P2.01-082 - Transcriptional Profiling Identified the Anti-Proliferative Effect of Mitofusin-2 Deficiency and Its Risk in Lung Adenocarcinoma (ID 6011)

      14:30 - 14:30  |  Author(s): Y. Lou

      • Abstract

      Background:
      Mitofusin-2(MFN2) was initially identified as a hyperplasia suppressor in hyper-proliferative vascular smooth muscle cells of hypertensive rat arteries, which has also been implicated in various cancers. There exists a controversy in whether it is an oncogene or exerting anti-proliferative effect on tumor cells. Our previous cell cycle analysis and MTT assay showed that cell proliferation was inhibited in MFN2 deficient A549 human lung adenocarcinoma cells, without investigating the changes in regulatory network or addressing the underlying mechanisms.

      Methods:
      We performed expression profiling in MFN2 knock-down A549 cells. Furthermore, we compared the expression profiling of a cohort consisting of 61 pairs of tumor-normal match samples from The Cancer Genome Atlas(TCGA).

      Results:
      The expression profiling in MFN2 knock-down cells suggested that cancer related pathways were among the most susceptible pathways to MFN2 deficiency. Next, we teased out the specific pathways to address the impact that MFN2 ablation had on A549 cells, as well as identified a few genes whose expression level associated with clinicopathologic parameters. In addition, transcriptional factor target enrichment analysis identified E2F as a potential transcription factor that was deregulated in response to MFN2 deficiency. Figure 1 Figure 2





      Conclusion:
      The anti-proliferative effect of MFN2 deficiency and its risk in lung adenocarcinoma were found by transcriptional profiling.