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Yuqing Lou

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    P1.03 - Biology (Not CME Accredited Session) (ID 935)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.03-22 - MiR-125b Plays a Tumor Suppressor Role in Inflammation-Related Non-Small Cell Lung Cancer via Repressing IGF-1 Signal Pathway (ID 11752)

      16:45 - 18:00  |  Author(s): Yuqing Lou

      • Abstract
      • Slides


      Epidemiologic data have indicated that chronic inflammation was highly associated with the pathogenesis of lung cancer. However, the molecular relations between inflammation and lung cancer have not been well understood. MicroRNAs could connect the inflammatory response with tumorigenesis through regulating their cancer-related targets. The aim of the present study was to identify the core miRNA in inflammation-related lung cancer and its potential mechanisms.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      RT-PCR was used to detect the expression of miRNAs and mRNAs. CKK8 and flow cytometry assays was performed for the function experiments. Microarray analysis and IPA analysis were used to predict the potential signal pathway.

      4c3880bb027f159e801041b1021e88e8 Result

      Mir-125b was the most dramatically up-regulated miRNAs after treated with IFN-r, whereas after stimulated with IL-10, mir-125b was the most strikingly down-regulated ones. Restoration of mir-125b expression could completely overrode the impact of IL-10 on both cell proliferation and apoptosis in NSCLC cell lines(Figure1). And the level of mir-125b was significantly lower in 30 NSCLC tumor tissues compared with normal controls (P<0.0001). Microarray analysis found 69 up-regulated genes and 105 down-regulated genes after down-regulate mir-125b. And IPA analysis indicated that IGF-1 signaling pathway was dramatically activated. The results were validated by RT-PCR.

      8eea62084ca7e541d918e823422bd82e Conclusion

      MiR-125b might play a tumor suppressor role via inhibiting IGF-1 signaling in inflammation-related lung cancer.


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