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H.S. Ock
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P3.02 - Biology/Pathology (ID 620)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.02-097b - Significance of PAK1/CREB Pathway in Lung Adenocarcinoma Oncogenesis (ID 10016)
09:30 - 09:30 | Author(s): H.S. Ock
- Abstract
Background:
P21-activated kinase 1 (PAK1) is serine/threonine protein kinase that contributes to Ras-driven tumorigenesis in non-small cell lung cancer (NSCLC). Cyclic AMP-response element-binding protein (CREB) is the transcription factor that regulates tumor cell differentiation and proliferation. Several studies have shown that expression level of PAK1 and CREB is elevated in NSCLC, respectively. However, the association between PAK1 and CREB in the regulation of carcinogenesis has not been well known in NSCLC. Here, we identified that overexpression of PAK1 and CREB is more prevalent in lung adenocarcinoma compared to normal tissue and PAK1 expression is significantly associated with CREB expression.
Method:
Sixteen tumor tissues from patients with lung adenocarcinoma were collected to evaluate PAK1 and CREB expressions by immunostaining and western blot analysis. Knockdown of PAK1 by siRNA was performed to evaluate the association between PAK1 and CREB.
Result:
PAK1 and CREB expressions, which were evaluated by immunohistochemistry and western blot assay were significantly increased in lung adenocarcinoma compared to normal lung tissues. Kaplan-Meier survival analysis with a online database showed the prognostic significance of PAK1 and CREB in lung adenocarcinoma. Knockdown of PAK1 by siRNA significantly suppressed the expression of CREB. PAK1 expression level was linearly correlated with CREB expression level by regression analysis (p=0.013).
Conclusion:
We demonstrated that expression level of both PAK1 and CREB was elevated in lung adenocarcinoma and high expression predicted a poor prognosis. Our results suggest that PAK1 regulates carcinogenesis through CREB in lung adenocarcinoma.