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X. Gao
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P1.05 - Poster Session with Presenters Present (ID 457)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Early Stage NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/05/2016, 14:30 - 15:45, Hall B (Poster Area)
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P1.05-024 - Preoperative Neuron-Specific Enolase to Albumin Ratio is a Prognostic Biomarker for Patients with Operable Non-Small-Cell Lung Cancer (ID 5273)
14:30 - 14:30 | Author(s): X. Gao
- Abstract
Background:
Neuron-specific Enolase (NSE) is a widely used tumor biomarker in small-cell lung cancer (SCLC) diagnosis, and serum albumin (Alb) levels are commonly used as indicators of the nutritional status of cancer patients. However, the prognostic value of these markers in combination has not been examined. This study was designed to explore the value of the combination between NSE and Alb in non-small-cell lung cancer (NSCLC).
Methods:
We retrospectively evaluated the prognostic value of the preoperative NSE to albumin ratio (NAR) in 319 patients with operable NSCLC. We analyzed associations among the NAR, clinicopathological characteristics, and inflammatory biomarkers. Univariate and multivariate analyses were performed to identify the clinicopathological characteristics associated with OS. Furthermore, we compared the prognostic value of the NAR with other established prognostic indexes by evaluating the area under the curves (AUC).
Results:
The optimal NAR cutoff level was found to be 3.2×10[-7]. We found that a higher NAR was associated with more advanced TNM staged cancers (P=0.041) and higher tumor stage (P=0.011).The NAR was also associated with the inflammatory biomarker albumin/globulin ratio (AGR, P=0.032), but not the neutrophil/lymphocyte ratio (NLR, P=0.295) or platelet/lymphocyte ratio (PLR, P=0.260). In multivariate analyses, the NAR was an independent prognostic factor for NSCLC patients (P<0.001). The AUC of the NAR was higher than the NLR, PLR or AGR at 24 and 36 months of follow-up.
Conclusion:
The preoperative NAR might be an independent prognostic factor for patients with operable NSCLC, and a higher NAR indicates a poorer prognosis.
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P3.01 - Poster Session with Presenters Present (ID 469)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.01-063 - XIAP Inhibits Mature Smac Induced Apoptosis by Degrading It through Ubiquitination in NSCLC (ID 5287)
14:30 - 14:30 | Author(s): X. Gao
- Abstract
Background:
X-linked inhibitor of apoptosis protein (XIAP) and second mitochondrial-derived activator of caspase (Smac) are two important prognostic biomarkers for cancer. They are negatively correlated in many types of cancers. However, their relationship is still unknown in lung cancer.
Methods:
RT-PCR and Western blot were performed to explore the correlation between Smac and XIAP at the level of mRNA and protein in NSCLC patients. Full-length XIAP, Smac and mature Smac were generated by PCR and cloned into pcDNA3.0-Flag/Myc. The location of mature Smac and full-length Smac was detected by immunofluorescence. MTT assay and Flow cytometry were detected the cell viability and apoptosis of transfected cells. Caspase-3 activity was masured by Caspase-3 activity assay. Co-immunoprecipitation assay was done to reveal the direct relation between XIAP and Smac. Nude mouse xenograft experiment further proved the relation and the function of Smac and XIAP in vivo.
Results:
In this study, we found that there was a negative correlation between Smac and XIAP at the level of protein but not mRNA in NSCLC patients. However, XIAP overexpression had no effect on degrading endogenous Smac in lung cancer cell lines. Therefore, we constructed plasmids with full length of Smac (fSmac) and mature Smac (mSmac) which located in cytoplasm instead of original mitochondrial location, and confirmed by immunofluorescence. Subsequently, we found that mSmac rather than fSmac was degraded by XIAP and inhibited cell viability. CHX chase assay and ubiquitin assay were performed to illustrate XIAP degraded mSmac through ubiquitin pathway. Overexpression of XIAP partially reverted apoptotic induction and cell viability inhibition by mSmac, which was due to inhibiting caspases-3 activation. In nude mouse xenograft experiments, mSmac inhibited Ki67 expression and slowed down lung cancer growth, while XIAP partially reversed the effect of mSmac by degrading it.
Conclusion:
In conclusion, XIAP inhibits mature Smac-induced apoptosis by degrading it through ubiquitination in NSCLC.
