NDLI: Mitofusin-2 over-expresses and leads to dysregulation of cell cycle and cell invasion in lung adenocarcinoma.

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Mitofusin-2 over-expresses and leads to dysregulation of cell cycle and cell invasion in lung adenocarcinoma.

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Mitofusin-2 over-expresses and leads to dysregulation of cell cycle and cell invasion in lung adenocarcinoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lou, Yuqing Li, Rong Liu, Jielin Zhang, Yanwei Zhang, Xueyan Jin, Bo Liu, Ya Wang, Zuoguang Zhong, Hua Wen, Shaojun Han, Baohui
Description	Author Affiliation: Lou Y ( Department of Pulmonary, Shanghai Chest Hospital, Shanghai Jiaotong University, 241 West Huaihai Road, Shanghai, 200030, People's Republic of China.)
Abstract	Mitofusin-2 (MFN2) is a mitochondrial protein associated with mitochondrial fusion process. It was initially identified as a hyperplasia suppressor and implicated in Charcot-Marie-Tooth disease. Recent studies showed that MFN2 played important roles in the development of multiple tumors. Here we examined MFN2 expression in 30 lung adenocarcinoma samples and revealed that the expression of MFN2 was significantly higher in lung adenocarcinoma tissues as compared to adjacent normal tissues. We then investigated the impact of MFN2 knockdown on A549 human lung adenocarcinoma cells and showed that cell proliferation, cell cycle and invasion behavior were all deregulated by MFN2 knockdown. And deregulation of cell cycle pathway after MFN2 knockdown was confirmed by microarray analysis. Furthermore, microarray analysis also revealed that different oncogenes such as RAP1A, RALB and ITGA2 were oppositely regulated by MFN2, which provided molecular clues for the paradoxical functions of MFN2 in tumor development. Taken together, our study unraveled the tumor-promoting functions of MFN2 in lung adenocarcinoma and implicated that the role of MFN2 in cancer development might be more complicated than expected and should be explored in detail in the future.
File Format	HTM / HTML
ISSN	13570560
Issue Number	4
Volume Number	32
e-ISSN	1559131X
Journal	Medical Oncology
Language	English
Publisher	Springer
Publisher Date	2015-04-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Adenocarcinoma Research Support, Non-u.s. Gov't Cell Proliferation Prognosis Gtp Phosphohydrolases Humans Middle Aged Male Mitochondrial Proteins Lung Neoplasms Antagonists & Inhibitors Immunoenzyme Techniques Journal Article Flow Cytometry Genetics Female Tumor Cells, Cultured Discipline Oncology Rna, Small Interfering Rna, Messenger Real-time Polymerase Chain Reaction Metabolism Reverse Transcriptase Polymerase Chain Reaction Cell Adhesion Blotting, Western Pathology Cell Cycle Neoplasm Staging Cell Movement Apoptosis
Content Type	Text
Resource Type	Article
Subject	Hematology Cancer Research Oncology

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