A novel BMX variant promotes tumor cell growth and migration in lung adenocarcinoma
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Ye Wang1,2,3, Jufeng Xia1,2,3, Zhaoyuan Fang1,2,3, Fei Li1,2,3, Duo Li1,2,3, Zuoyun Wang1,2,3, Yan Feng1,2,3, Jian Zhang1,2,3, Haiquan Chen6,7, Hongbin Ji1,2,3,5, Hongyan Liu1,2,3,4
1CAS Key Laboratory of Systems Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Science, Shanghai, 200031, China
2CAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Science, Shanghai, 200031, China
3Innovation Center for Cell Signaling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Science, Shanghai, 200031, China
4Institute of Basic Medicine, Shandong Academy of Medical Sciences, Jinan, 250062, Shandong, China
5School of Life Science and Technology, Shanghai Tech University, Shanghai, 200120, China
6Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China
7Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China
Hongyan Liu, email: [email protected]
Hongbin Ji, email: [email protected]
Keywords: lung adenocarcinomas, BMXΔN, cell proliferation, migration, skipping variant
Received: January 12, 2017 Accepted: March 22, 2017 Published: April 03, 2017
The non-receptor tyrosine kinase BMX has been reported in several solid tumors. However, the alternative splicing of BMX and its clinical relevance in lung cancer remain to be elucidated. Exon1.0 array was used to identify a novel alternative splicing of BMX, BMXΔN, which was confirmed by rapid amplification of cDNA ends and reverse transcription-polymerase chain reaction. BMXΔN, resulting from exon skipping with excluding exon 1 to exon 8 of BMX gene, was found in 12% human lung adenocarcinoma specimens. BMXΔN is not found in paired pathologically normal lungs and positively correlated with EGFR mutation in lung adenocarcinomas. Moreover, BMXΔN increases cell proliferation, neoplastic transformation, and migratory property of human non-small cell lung cancer cells. The function of BMXΔN in lung cancer might be presumably due to enhanced ERK signaling.
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