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Study on the Molecular Mechanisms of dlk1 Stimulated Lung Cancer Cell Proliferation

Author(s): Yu LIU | Jinjing TAN | Lin LI | Shuo LI | Shuangmei ZOU | Ying ZHANG | Xiaojing ZHANG | Bing LING | Naijun HAN | Suping GUO | Yanning GAO

Journal: Chinese Journal of Lung Cancer
ISSN 1009-3419

Volume: 13;
Issue: 10;
Start page: 923;
Date: 2010;
Original page

Keywords: dlk1 | Lung neoplasms | Proliferation | CyclinB1

Background and objective The imprinted gene dlk1 has been recognized as a cancer related gene since it aberrantly expressed in a series of cancer tissues, but its role in lung cancer is still unknown. The aim of this study is to examine dlk1’s expression in non-small cell lung cancers (NSCLCs) and investigate the molecular mechanism by which dlk1 could accelerate the proliferation of the cells in lung cancer cell lines (H520). Methods The relative expression of dlk1 among 30 NSCLC specimens and their adjacent normal lung tissues were analyzed by RT-PCR. A cell model that stably expressed exogenous dlk1 was established following that the dlk1 gene was cloned into a eukaryotic expression vector and then transfected into the lung cancer cells H520. CCK8 analysis and colony forming assay were employed to investigate the effect of dlk1 on cell proliferation. The expression of CyclinB1 was detected by Western blot. Results dlk1 aberrantly expressed in 36.7% (11/30) of the tumor tissues of NSCLC compared with their adjacent cancer lung tissues. CCK8 analysis showed that overexpression of dlk1 could promote the proliferation of H520 cells (P < 0.05) and the results was further confirmed by colony forming assay. Western blot analysis found that over expression of dlk1 could up-regulate the expression of CyclinB1 (P < 0.05). Conclusion dlk1 aberrantly expressed in NSCLCs. The Overexpression of dlk1 could accelerate the proliferation of lung cancer cells H520 in vitro, probably through up-regulating the expression of cell cycle protein CyclinB1.

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