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The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating Wnt/β-catenin pathway.

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Pubmed体系：
作者：
Xuebing Li[1,*1] ; Xuexia Zhou[2] ; Feng Hua[3] ; Yaguang Fan[1] ; Lingling Zu[1] ; Yuli Wang[1] ; Wang Shen[1] ; Hongli Pan[1] ; Qinghua Zhou[1,4,*1] ;
机构： [1]Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute,Tianjin Medical University General Hospital, Tianjin, P. R. China [2]Department of Neuropathology, Tianjin KeyLaboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, TianjinMedical University General Hospital, Tianjin, P. R. China [3]Department of Thoracic Surgery, Shandong Cancer Hospitaland Institute, Jinan, P. R. China [4]Sichuan Lung Cancer Institute, Sichuan Lung Cancer Center, West ChinaHospital, Sichuan University, Chengdu, P. R. China
出处：

关键词： Sam68 NSCLC cell proliferation Wnt/β-catenin signaling

摘要：
Src associated in mitosis, 68 kDa (Sam68) is a KH domain RNA-binding protein that regulates a broad scope of biological events, including RNA metabolism, transcription and signal transduction. Herein, we aimed to explore the expression, clinical significance and biological function of Sam68 in human non-small cell lung cancer (NSCLC). By applying quantitative real-time PCR (qRT-PCR), western blotting and immunohistochemistry (IHC) methods, we found that nucleic localized Sam68 was markedly overexpressed in NSCLC tissues and cell lines. By X2 analysis and Kaplan-Meier survivial analysis between Sam68 expression and various clinicopathological features, Sam68 was found to be significantly associated with clinical T stage, advanced tumor grade, and short overall survival. Finally, in vitro loss-of-function studies showed that knockdown of Sam68 inhibited cell proliferation, colony formation and cell cycle progression in NSCLC cells. Moreover, our results clarified that knockdown of Sam68 could suppress NSCLC cell proliferation via the inhibition of Wnt/β-catenin pathway. To conclude, our results demonstrated that upregulation of Sam68 in NSCLC resulted in poor prognosis, and it promoted cell proliferation via activating Wnt/β-catenin signaling pathway, which could serve as a novel biomarker for the prognosis and therapy of NSCLC. IJCEP Copyright © 2017.

基金：
the National Natural Science Foundation of China (No. 81572288, to Qinghua Zhou; No. 81302002, to Xuebing Li; No. 81502166, to Xuexia Zhou), the Key Project of International Cooperation of Science and Technology Innovation between Governments, the National Key Research and Development Plan of China (No. 2016YEE0103400, to Qinghua Zhou), the Tianjin Natural Science Foundation (No. 14JCQNJC12300, to Xuebing Li; No. 17JCYBJC2- 7100, to Xuexia Zhou; No. 17JCQNJC11700, to Hongli Pan; No. 17JCYBJC25400, to Yaguang Fan), and the “New Century” Talent Training Project of Tianjin Medical University General Hospital (2014, to Xuebing Li; 2016, to Xuexia Zhou).
语种：
外文
PubmedID：
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出版当年[2017]版：
大类 | 4 区 医学
小类 | 4 区 肿瘤学 4 区 病理学
最新[2023]版：
无
第一作者：
第一作者机构： [1]Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute,Tianjin Medical University General Hospital, Tianjin, P. R. China [*1]Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, No. 154 Anshan Street, Heping District, Tianjin 300052, P. R. China
通讯作者：
通讯机构： [1]Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute,Tianjin Medical University General Hospital, Tianjin, P. R. China [4]Sichuan Lung Cancer Institute, Sichuan Lung Cancer Center, West ChinaHospital, Sichuan University, Chengdu, P. R. China [*1]Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, No. 154 Anshan Street, Heping District, Tianjin 300052, P. R. China
推荐引用方式(GB/T 7714)：
Xuebing Li,Xuexia Zhou,Feng Hua,et al.The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating Wnt/β-catenin pathway.[J].International journal of clinical and experimental pathology.2017,10(8):8281-8291.
APA：
Xuebing Li,Xuexia Zhou,Feng Hua,Yaguang Fan,Lingling Zu...&Qinghua Zhou.(2017).The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating Wnt/β-catenin pathway..International journal of clinical and experimental pathology,10,(8)
MLA：
Xuebing Li,et al."The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating Wnt/β-catenin pathway.".International journal of clinical and experimental pathology 10..8(2017):8281-8291

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