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Lung Cancer: Late-Breaking Abstracts: Lung Cancer Mechanisms |

RBM5 Inhibits the Proliferation of Cigarette Smoke-Induced Cancerous Transformation of BEAS-2B Cells FREE TO VIEW

Zhang Jie, PhD; Lv Xuejiao, PhD; Hao Yuqiu, PhD; Su Zhenzhong, PhD; Meng Guangping, PhD; Wang Qi, PhD; Zhang Lin, PhD
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The Second Affiliated Hospital of Jilin University, Changchun, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A257. doi:10.1016/j.chest.2016.02.269
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SESSION TITLE: Late-Breaking Abstracts: Lung Cancer Mechanisms

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Sunday, April 17, 2016 at 08:30 AM - 09:30 AM

PURPOSE: Cigarette smoking is the most important risk factor of lung cancer, and greater than 90% of lung cancers are cigarette smoke-related. Recent studies have indicated that the RNA-binding motif protein 5 (RBM5) has the ability to suppress tumor growth. The aim of this study was to investigate the role of RBM5 in cigarette-smoke extract (CSE)-induced cancerous transformation of bronchial epithelial cells and its regulation mechanism.

METHODS: We treated BEAS-2B cells for 8 days with CSE concentrations (0, 25, 50, 100μg/mL) or DMSO followed by a recovery period of two weeks. We successfully established an in vitro model of CSE-induced cancerous transformation of BEAS-2B cells. Then, the cells were transfected with LV-RBM5. Cell morphologic changes were assessed using a phase-contrast microscope. Proliferation ability of cells were examined using MTT and Colony Formation assay. Cell cycling and apoptosis was determined by flow cytometry. Expression of cell cycle and apoptosis genes were examined at both the RT-PCR and Western blot.

RESULTS: Our findings have shown that expression of RBM5 were obviously down-regulated in cancerous transformed BEAS-2B cells. RBM5 overexpression significantly inhibited the proliferation, induced G1/S arrest, and triggered the apoptosis of CSE-induced cancerous transformation bronchial epithelial cells.

CONCLUSIONS: In this study, we established a model in which the early stages of CSE-induced tumorigenesis to determine RBM5 function, and concluded that RBM5 inhibited growth of CSE-induced cancerous transformation BEAS-2B cells through cell cycle arrest, apoptosis, which suggests that RBM5 plays an important role in the pathogenesis of smoking related cancer.

CLINICAL IMPLICATIONS: It is possible that an understanding of regulatory mechanism of RBM5 in smoking related lung cancer will lead to the development of new therapies.

DISCLOSURE: The following authors have nothing to disclose: Zhang Jie, Lv Xuejiao, Hao Yuqiu, Su Zhenzhong, Meng Guangping, Wang Qi, Zhang Lin

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