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Lei Zhao
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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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P1.03-21 - Huaier Aqueous Extract Induces Lung Adenocarcinoma Cell Apoptosis Through Excessive Activation Of MEK/ERK Signaling Pathway (ID 12019)
16:45 - 18:00 | Author(s): Lei Zhao
- Abstract
Background
As the most important pathological types of lung cancer, adenocarcinoma has poor prognosis due to the characteristics of early metastasis and recurrence even in effective surgery, radiotherapy and chemotherapy. In China, Traditional Chinese medicine “Huaier aqueous extract” (HAE) is widely used in antineoplastic treatment, but its molecular mechanism in lung adenocarcinoma remains unclear. This study aimed to explore the apoptotic mechanism of HAE in lung adenocarcinoma.
a9ded1e5ce5d75814730bb4caaf49419 Method
MTT assay and flow-cytometric analysis were measured to identify the cell viability and apoptosis rate affected by HAE in human lung adenocarcinoma A549, H322 cell. Immunofluorescence assay was applied to examine the effect of HAE on expression and distribution of Cytochrome C and ERK1/2 in A549, H322 cell. Further, A549 cell was respectively treated with HAE and subjected to western blotting for protein level of MEK/ERK signaling pathway. In human trials, a total of 40 patients with stage I lung adenocarcinoma after complete resection were enrolled from January 2015 to December 2016. 20 of them were given HAE and others were not, and then the patients’ 3-year disease free survival was examined.
4c3880bb027f159e801041b1021e88e8 Result
HAE significantly inhibited the cell viability of A549, H322 cell in dose-dependent and time--dependent manner. Further, HAE induced accumulation of Cytochrome C, an apoptosis core factor, in cytoplasm and promote the apoptosis of A549, H322 cells. Meanwhile, HAE launched the expression of ERK1/2 and the latter migrated more to the nucleus following with excessive activation of MEK/ERK signaling pathway. The patients treated with HAE showed fewer recurrences than the rest (3-year disease free survival: 93.8% vs 71.4%; P=0.048).
8eea62084ca7e541d918e823422bd82e Conclusion
HAE could over-activate MEK/ERK signaling pathway and exert apoptosis-inducing effects in lung adenocarcinoma.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.03 - Biology (Not CME Accredited Session) (ID 952)
- 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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P2.03-23 - MicroRNA-30e Inhibits Cell Proliferation and Invasion in Non-Small Cell Lung Cancer via Directly Targeting SOX9 (ID 12848)
16:45 - 18:00 | Presenting Author(s): Lei Zhao
- Abstract
Background
Previous studies reported that microRNA-30e (miR-30e) was dysregulation in multiple human cancers. However, the expression, functions and molecular mechanism of miR-30e in NSCLC remains unknown. In this study, we found that miR-30e expressed at low levels in NSCLC tissues and NSCLC cell lines.
a9ded1e5ce5d75814730bb4caaf49419 Method
The miR-30e expression was texted in NSCLC tissues and cell lines by RT-qPCR. We then overexpressed miR-30e expression in NSCLC cells to evaluate its effects in regulating NSCLC proliferation and invasion in vitro. Moreover, the mechanisms underlying the biological roles of miR-30e in NSCLC were investigated using luciferase reporter assay.
4c3880bb027f159e801041b1021e88e8 Result
In NSCLC cell lines, enforced expression of miR-30e inhibited cell proliferation and invasion in vitro. In addition, miR-30e negatively regulated SOX9 expression through directly binding to the 3'UTR of SOX9, and an inverse correlation was found between miR-30e and SOX9 mRNA expression level in NSCLC tissues. Moreover, SOX9 knockdown led to decreased proliferation and invasion of NSCLC cells.
8eea62084ca7e541d918e823422bd82e Conclusion
miR-30e is downregulated in NSCLC and inhibits cell proliferation and invasion, possibly by directly targeting SOX9.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P3.03 - Biology (Not CME Accredited Session) (ID 969)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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P3.03-23 - A Propensity Score Matching Cohort Study on Prognosis of the Diversity of MUC1 Expression in Patients with Lung Adenocarcinoma (ID 13107)
12:00 - 13:30 | Author(s): Lei Zhao
- Abstract
Background
To probe the expression of MUC1 (Mucin-1) in lung adenocarcinoma tissues, and estimate the relationship between the expression level of MUC1 and prognosis or clinical pathological factors in patients with lung adenocarcinoma simultaneously, so as to establish personal therapeutic strategies and forecast prognosis.
a9ded1e5ce5d75814730bb4caaf49419 Method
A retrospective analysis was originally conducted on 182 lung adenocarcinoma patients who underwent surgical resection collected from July 2007 and September 2010 at the First Affiliated Hospital of Dalian Medical University. None of the patients received neoadjuvant therapy. Each tumor was reevaluated according to the current adenocarcinoma classification based on HE stains. Additional immunohistochemical staining for MUC1(Mucin-1) was used in selected cases. Cox proportional hazard regression model was used for univariate analysis. The confounding parameters were compromised by propensity score matching (PSM).
4c3880bb027f159e801041b1021e88e8 Result
Among 182 patients with lung adenocarcinoma, 107 patients were MUC1 low expressed, 44 patients were MUC1 moderate expressed 33 patients were MUC1 high expressed. We found the expression of MUC1 was significantly different in gender (p=0.014), smoking history (p=0.009), T stage (p=0.019), N stage (p=0.015), clinical stage (p=0.024) and the WHO classification of tumors of the lung adenocarcinoma (p=0.002). But we found all above differences among groups were no significance after PSM. Lung adenocarcinoma patients with high MUC1 expression, poorly differentiated and high pTNM stage had early relapse than the other (P≤0.05), no matter took PSM.
8eea62084ca7e541d918e823422bd82e ConclusionUnivariate analysis of clinical pathologic factors on disease-free survival risk. Clinical Factor
HR
95%CI
P value
Gender
male
1.000
fmale
0.732
0.437-1.226
0.236
Age
≤67
1.000
>67
0.928
0.562 -1.534
0.772
History of smoking
Out
1.000
Without
1.756
0.981 -3.140
0.058
Tumor size
≤2cm
1.000
>2cm
2.100
1.067- 4.135
0.032
Differentiation
Poor
1.000
Moderate
10.929
4.734- 25.232
<0.001
Well
3.151
1.376- 7.218
0.007
T stage
T1
1.000
T2
1.483
0.798- 2.757
0.213
T3
3.831
2.083- 7.048
<0.001
N stage
N0
1.000
N1
2.247
0.879- 5.744
0.091
N2
3.506
2.047- 6.006
<0.001
TNM stage
I
1.000
II
2.310
0.810- 6.591
0.118
III
3.823
2.272- 6.432
<0.001
Pathological subgroups
MIA
1.000
AP
3.414
1.146- 10.174
0.028
PA
1.486
0.600- 3.683
0.392
MPA
2.245
0.918- 5.494
0.076
SOP
5.566
1.116- 27.754
0.036
MU
5.148
0.617- 42.923
0.130
Lep
0.748
0.090- 6.210
0.788
MUC1 expression
Low
1.000
Moderate
1.235
0.604- 2.527
0.563
High
2.289
1.318- 3.974
0.003
MUC1 expression (PSM)
Low
1.000
Moderate
1.289
0.557- 2.985
0.553
High
2.462
1.142- 5.312
0.022
High expression of MUC1 can be a significant independent risk factors for predicting the prognosis of lung adenocarcinoma.
6f8b794f3246b0c1e1780bb4d4d5dc53