Journal
ONCOTARGET
Volume 8, Issue 20, Pages 33405-33415Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.16796
Keywords
lung adenocarcinomas; BMX Delta N; cell proliferation; migration; skipping variant
Categories
Funding
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB19000000]
- National Natural Science Foundation of China [81372509, 81325015, 81430066, 31621003, 81402276, 81402371, 81401898, 81402498, 81101583, 31370747]
- Science and Technology Commission of Shanghai Municipality [15XD1504000]
- Innovation Project of Shandong Academy of Medical Sciences
- Excellent Innovation Team of Shandong Academy of Medical Sciences, Shanghai Institutes for Biological Sciences [2014KIP304]
- Project for Laureate of Taishan Scholar [ts201511075]
- SA-SIBS scholarship program
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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, BMX Delta N, which was confirmed by rapid amplification of cDNA ends and reverse transcription-polymerase chain reaction. BMX Delta N, resulting from exon skipping with excluding exon 1 to exon 8 of BMX gene, was found in 12% human lung adenocarcinoma specimens. BMX Delta N is not found in paired pathologically normal lungs and positively correlated with EGFR mutation in lung adenocarcinomas. Moreover, BMX Delta N increases cell proliferation, neoplastic transformation, and migratory property of human non-small cell lung cancer cells. The function of BMX Delta N in lung cancer might be presumably due to enhanced ERK signaling.
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