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Int. J. Mol. Sci. 2018, 19(5), 1479; https://doi.org/10.3390/ijms19051479

B-Myb Mediates Proliferation and Migration of Non-Small-Cell Lung Cancer via Suppressing IGFBP3

1
Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, ChongQing Medical University, Chongqing 400016, China
2
Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
3
Department of Pathology, College of Basic Medical Sciences, Jiamusi University, Jiamusi 154007, China
4
Department of Cell Biology, College of Basic Medical Sciences, Jiamusi University, Jiamusi 154007, China
*
Author to whom correspondence should be addressed.
Received: 20 April 2018 / Revised: 6 May 2018 / Accepted: 11 May 2018 / Published: 16 May 2018
(This article belongs to the Special Issue Cell Growth Regulation)
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Abstract

B-Myb has been shown to play an important oncogenic role in several types of human cancers, including non-small-cell lung cancer (NSCLC). We previously found that B-Myb is aberrantly upregulated in NSCLC, and overexpression of B-Myb can significantly promote NSCLC cell growth and motility. In the present study, we have further investigated the therapeutic potential of B-Myb in NSCLC. Kaplan–Meier and Cox proportional hazards analysis indicated that high expression of B-Myb is significantly associated with poor prognosis in NSCLC patients. A loss-of-function study demonstrated that depletion of B-Myb resulted in significant inhibition of cell growth and delayed cell cycle progression in NSCLC cells. Notably, B-Myb depletion also decreased NSCLC cell migration and invasion ability as well as colony-forming ability. Moreover, an in vivo study demonstrated that B-Myb depletion caused significant inhibition of tumor growth in a NSCLC xenograft nude mouse model. A molecular mechanistic study by RNA-seq analysis revealed that B-Myb depletion led to deregulation of various downstream genes, including insulin-like growth factor binding protein 3 (IGFBP3). Overexpression of IGFBP3 suppressed the B-Myb-induced proliferation and migration, whereas knockdown of IGFBP3 significantly rescued the inhibited cell proliferation and motility caused by B-Myb siRNA (small interfering RNA). Expression and luciferase reporter assays revealed that B-Myb could directly suppress the expression of IGFBP3. Taken together, our results suggest that B-Myb functions as a tumor-promoting gene via suppressing IGFBP3 and could serve as a novel therapeutic target in NSCLC. View Full-Text
Keywords: B-Myb; IGFBP3; NSCLC; proliferation; motility B-Myb; IGFBP3; NSCLC; proliferation; motility
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Fan, X.; Wang, Y.; Jiang, T.; Cai, W.; Jin, Y.; Niu, Y.; Zhu, H.; Bu, Y. B-Myb Mediates Proliferation and Migration of Non-Small-Cell Lung Cancer via Suppressing IGFBP3. Int. J. Mol. Sci. 2018, 19, 1479.

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