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Xinyin Liu
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P2.01 - Advanced NSCLC (Not CME Accredited Session) (ID 950)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.01-69 - EZH2-Mediated Epigenetic Suppression Of GDF15 Predicts a Poor Prognosis and Regulates Cell Proliferation in Non-Small Cell Lung Cancer (ID 12457)
16:45 - 18:00 | Author(s): Xinyin Liu
- Abstract
Background
Growth differentiation factor 15 (GDF15), a member of the TGF-β superfamily of cytokines, has been reported to exert very heterogeneous functions in various tumors. However, the role of GDF15 and its underlying mechanism in mediating non-small cell lung cancer (NSCLC) progression remain unknown.
a9ded1e5ce5d75814730bb4caaf49419 Method
GDF15 expression level was analyzed in 66 NSCLC tissues by quantitative reverse transcription PCR (qRT-PCR). The effect of GDF15 on proliferation was evaluated by MTT and colony formation assays, flow cytometric analysis. NSCLC cells transfected with pcDNA-GDF15 or empty vector were injected into nude mice to study the effect of GDF15 on tumorigenesis in vivo. Chromatin immunoprecipitation (ChIP) assay was used to investigate the mechanism of action of GDF15 in the NSCLC cells.
4c3880bb027f159e801041b1021e88e8 Result
In this study, we found that GDF15 is down-regulated in paired NSCLC tissues and is correlated with poor clinical outcomes in NSCLC. Further experiments demonstrated that overexpression of GDF15 significantly repressed NSCLC proliferation both in vitro and in vivo. Mechanistic studies reveal that inhibition of EZH2 expression prevented its binding to the GDF15 promoter region and reduced the trimethylation modification pattern of H3K27.
8eea62084ca7e541d918e823422bd82e Conclusion
Together, our data uncover that GDF15 is a direct target of EZH2, and as a regulator of proliferation, might serve as a candidate prognostic biomarker and target for new therapies in human NSCLC.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.13 - Targeted Therapy (Not CME Accredited Session) (ID 962)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.13-34 - Long Intergenic Non-Coding RNA 00665 Induces Acquired Resistance to Gefitinib in Non-Small-Cell Lung Cancer (ID 11903)
16:45 - 18:00 | Author(s): Xinyin Liu
- Abstract
Background
Gefitinib, a tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR-TKI), has been used as the first choice of treatment for advanced non-small cell lung cancer (NSCLC). However, during the course of treatment cancer cells often develop resistance to gefitinib without fully understood mechanisms. In recent years, numerous studies have shown that long non-coding RNAs (lncRNAs) play vital roles in modulating various biological processes, such as cell apoptosis, proliferation, migration, and invasion. Nevertheless cancer drug resistance mechanisms related to LncRNAs and their important roles in cancer development are still poorly understood. In this study, we aimed to elucidate an important role of long intergenic non-coding RNA 00665 (LINC00665) in developing resistance to gefitinib in NSCLC.
a9ded1e5ce5d75814730bb4caaf49419 Method
Quantitative reverse transcription PCR (qRT-PCR) was performed to examine the expression levels of LINC00665 in 10 pairs of LUAD tissues from patients who had never been treated with gefitinib (NG) and those who were treated with gefitinib but developed resistance (GR). The effect of LINC00665 on proliferation and apoptosis in gefitinib-resistant cells was evaluated by CCK8, colony formation, flow-cytometric analysis and in vivo tumor formation assays. Western-blot and immunohistochemistry were used to evaluate the expression of EGFR and its downstream event.
4c3880bb027f159e801041b1021e88e8 Result
LINC00665 expression levels were significantly increased in NSCLC patients who developed acquired resistance to gefitinib compared to the NG group.Furthermore, LINC00665 inhibition reversed gefitinib sensitivity both in vitro and in vivo by suppressing cell growth and induced cell apoptosis. Importantly, knockdown of LINC00665 marked decreased activation of EGFR and its downstream event Akt and ERK1/2.
8eea62084ca7e541d918e823422bd82e Conclusion
Taken together,our study demonstrates that LINC00665 may be a potential biomarker of response to gefitinib as well as a novel therapeutic target for future treatment of NSCLC.
6f8b794f3246b0c1e1780bb4d4d5dc53
