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S. Yang
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P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 3
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.04-083 - The Metastasis-Related Noncoding RNA Expression Profile and LncRNA LOC101448202 Induces 95D Cell Migration and Tumor Growth (ID 1640)
09:30 - 17:00 | Author(s): S. Yang
- Abstract
Background:
Metastasis of non-small cell lung cancer shortens the survival time of patients and decreases their quality of life. This unfortunate situation could be improved if the functions of long noncoding RNAs (lncRNAs) were identified in depth.
Methods:
not applicable
Results:
In the present study, a large number of lncRNAs and mRNAs with different expression patterns were verified in 95D and 95C lung cancer cell lines. The lncRNA, LOC101448202, was highly expressed in 95D cells, and lentivirus-mediated RNA interference was able to silence its expression with a silencing efficiency of 92%. LOC101448202 gene silencing led to a decrease in cell proliferation, adhesion, migration, and invasion and the number of pseudopods and microvillion the cell surface was also reduced. At the mRNA level, her-2 expression was inhibited and the expression of nm23-H1 and E-cadherin was increased. At the protein level, β-catenin and ezrin levels were decreased both in vitro and in vivo. In clinical specimens and mouse models, LOC101448202 expression was positively related to tumor growth.
Conclusion:
These data indicate that LOC101448202 expression levels are associated with 95D cell metastasis, demonstrating the tumor-promoting function of this lncRNA.
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P1.04-085 - The Role and Potential Mechanisms of LncRNA-TATDN1 in the Metastasis and Invasion of 95D Cell (ID 1675)
09:30 - 17:00 | Author(s): S. Yang
- Abstract
Background:
The invasion and metastasis of malignant cell is generally considered as a major reason why it is always failed in the therapy of lung cancer. The mechanism in metastasis is complicated and uncertain as well. The scientific research proves that Long non-coding RNA (LncRNA) is bound up with the occurrence, development and prognoses of lung cancer.
Methods:
Application of high throughput LncRNA chip to investigate the differentially expressed LncRNA between 95D and 95C cell lines. RNA interference (RNAi) approaches were used for the analysis of the biological functions and metastasis of TATDN1. Tumor growth was studied in nude mice.
Results:
TATDN1-1 was highly expressed in 95D cells lines and NSCLC tissues. In 95D cells knockdown of TATDN1 by using small interfering RNA (siRNA) resulted in significant reduction in proliferation, adhesion, migration and invasion of these cells in vitro. 95D cells xenografts with decreased TATDN1 expression were impaired in tumor formation and growth. On genetic level, MALAT-1displays the strongest association with genes involved in cancer like cellular growth, movement, proliferation, signaling.
Conclusion:
These data indicate that TATDN1expression levels are associated with 95D cells metastasis and identify tumor-promoting functions of TATDN1.
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P1.04-116 - The Role of JAK/STAT3 Signaling Pathway on Apoptosis of Lung Adenocarcinoma Cell Line PC-9 Induced by Icotinib (ID 2263)
09:30 - 17:00 | Author(s): S. Yang
- Abstract
Background:
The aim of the study is to estimate the role of JAK/STAT3 signaling pathway on apoptosis of lung adenocarcinoma induced by icotinib.
Methods:
EGFR mutation was detected in lung adenocarcinoma cell line PC-9 by ARMS assay; The inhibitory rates of cell proliferation, at different concentrations (0 ~ 100 umol/L) of icofinib and continued incubating for 24，48 and 72 h respectively, were evaluated by MTT assay; Apoptosis of PC-9 cells exposured to different concentrations of icotinib(0, 0.1, 1 and 10 umol/L) for 48 h were evaluated by TUNEL assay; JAK2, STAT3, Bcl-2, Bax mRNA expressions were evaluated by Real-time PCR assay; The protein levels of P-STAT3 and IL-6 were evaluated by Western-blot assay.
Results:
Human lung adenocarcinoma cell line PC-9 had an exon 19 deletion mutation in EGFR gene; Followed by treatment of icotinib，the proliferation of PC-9 cells were all inhibited significantly, especially in 48 and 72 h (P<0.01) in all concentrations; The inhibitory rates of cell proliferation in different treating time had statistical significance (P<0.01); Cell apoptosis at different concentrations were increased significantly (P<0.05); Along with the increasing concentrations, gen expression levels of JAK2, STAT3 and Bcl-2 decreased significantly (P<0.05), Bax increased significantly (P<0.05), JAK2/STAT3 ratios increased significantly (P<0.01), and Bcl-2/bax ratios decreased significantly (P<0.01); P-STAT3 and IL-6 protein levels were inhibited significantly at by higher concentration.
Conclusion:
JAK/STAT3 signaling pathway take a participate in apoptosis of PC-9 cells induced by icotinib. The most likely mechanism is icotinib inhibited the gen expression levels of JAK2, STAT3 and Bcl-2, so with the P-STAT3 and IL-6 protein levels, and mediated gene Bax overexpression.
