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Int. J. Mol. Sci. 2017, 18(6), 860;

B-Myb Is Up-Regulated and Promotes Cell Growth and Motility in Non-Small Cell Lung Cancer

Department of Biochemistry and Molecular Biology, Chongqing Medical University, 1# Yixueyuan Road, Yuzhong District, Chongqing 400016, China
Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
Authors to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 9 March 2017 / Revised: 26 March 2017 / Accepted: 5 April 2017 / Published: 27 May 2017
(This article belongs to the Collection Advances in Molecular Oncology)
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B-Myb is a transcription factor that is overexpressed and plays an oncogenic role in several types of human cancers. However, its potential implication in lung cancer remains elusive. In the present study, we have for the first time investigated the expression profile of B-Myb and its functional impact in lung cancer. Expression analysis by quantificational real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry demonstrated that B-Myb expression is aberrantly overexpressed in non-small cell lung cancer (NSCLC), and positively correlated with pathologic grade and clinical stage of NSCLC. A gain-of-function study revealed that overexpression of B-Myb significantly increases lung cancer cell growth, colony formation, migration, and invasion. Conversely, a loss-of-function study showed that knockdown of B-Myb decreases cell growth, migration, and invasion. B-Myb overexpression also promoted tumor growth in vivo in a NSCLC xenograft nude mouse model. A molecular mechanistic study by RNA-sequencing (RNA-seq) analysis showed that B-Myb overexpression causes up-regulation of various downstream genes (e.g., COL11A1, COL6A1, FN1, MMP2, NID1, FLT4, INSR, and CCNA1) and activation of multiple critical pathways (e.g., extracellular signal-regulated kinases (ERK) and phosphorylated-protein kinase B (Akt) signaling pathways) involved in cell proliferation, tumorigenesis, and metastasis. Collectively, our results indicate a tumor-promoting role for B-Myb in NSCLC and thus imply its potential as a target for the diagnosis and/or treatment of NSCLC. View Full-Text
Keywords: B-Myb; lung cancer; proliferation; migration; extracellular signal-regulated kinases (ERK) B-Myb; lung cancer; proliferation; migration; extracellular signal-regulated kinases (ERK)

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Jin, Y.; Zhu, H.; Cai, W.; Fan, X.; Wang, Y.; Niu, Y.; Song, F.; Bu, Y. B-Myb Is Up-Regulated and Promotes Cell Growth and Motility in Non-Small Cell Lung Cancer. Int. J. Mol. Sci. 2017, 18, 860.

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