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Mol. Cells 2010; 30(4): 355-362

Published online October 31, 2010

https://doi.org/10.1007/s10059-010-0134-8

© The Korean Society for Molecular and Cellular Biology

c-Myc Stimulates Cell Invasion by Inhibiting FBX8 Function

Hyun Jung Cho, Yun Jeong Oh, Junhye Kwon1, Jae Young Kwon, Kyung-Soo Kim2, and Hongtae Kim*

Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea, 1Department of Biological Sciences, Sookmyung Women’s University, Seoul 140-742, Korea, 2Department of Family Medicine, Seoul St. Mary’s Hospital, The Catholic University of Korea, College of Medicine, Seoul 137-040, Korea

Correspondence to : *Correspondence: khtcat@skku.edu

Received: April 15, 2010; Revised: August 2, 2010; Accepted: August 12, 2010

Abstract

c-Myc is a cellular onco-protein and a transcriptional activator important for cell growth, cell division, and tumorigenesis. Despite all that is known of its function, the mechanism of how c-Myc contributes to tumorigenesis is unclear. To gain insight into the mechanism through which c-Myc protein exerts its oncogenic activity, we performed large-scale, tandem repeat affinity purification and identified the F box only protein 8 (FBX8), an F-box and Sec7 domain-containing protein, as a novel Myc-binding protein. The c-Myc/FBX8 interaction was mediated by the c-Myc box II (MBII) region. We also confirmed that Myc protein overexpression in 293T cells affected FBX8 cellular trans-location and led to recovery from FBX8-mediated inhibi-tion of ADP-ribosylation factor 6 (ARF6) function during cell invasion. Together, these results suggest that FBX8 is a novel c-Myc binding protein and that c-Myc induces cell invasive activity through the inhibition of FBX8 effects on ARF6 function during cell invasion.

Keywords c-Myc, cell invasion, FBX8, tumorigenesis, ubiquitination

Article

Research Article

Mol. Cells 2010; 30(4): 355-362

Published online October 31, 2010 https://doi.org/10.1007/s10059-010-0134-8

Copyright © The Korean Society for Molecular and Cellular Biology.

c-Myc Stimulates Cell Invasion by Inhibiting FBX8 Function

Hyun Jung Cho, Yun Jeong Oh, Junhye Kwon1, Jae Young Kwon, Kyung-Soo Kim2, and Hongtae Kim*

Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea, 1Department of Biological Sciences, Sookmyung Women’s University, Seoul 140-742, Korea, 2Department of Family Medicine, Seoul St. Mary’s Hospital, The Catholic University of Korea, College of Medicine, Seoul 137-040, Korea

Correspondence to:*Correspondence: khtcat@skku.edu

Received: April 15, 2010; Revised: August 2, 2010; Accepted: August 12, 2010

Abstract

c-Myc is a cellular onco-protein and a transcriptional activator important for cell growth, cell division, and tumorigenesis. Despite all that is known of its function, the mechanism of how c-Myc contributes to tumorigenesis is unclear. To gain insight into the mechanism through which c-Myc protein exerts its oncogenic activity, we performed large-scale, tandem repeat affinity purification and identified the F box only protein 8 (FBX8), an F-box and Sec7 domain-containing protein, as a novel Myc-binding protein. The c-Myc/FBX8 interaction was mediated by the c-Myc box II (MBII) region. We also confirmed that Myc protein overexpression in 293T cells affected FBX8 cellular trans-location and led to recovery from FBX8-mediated inhibi-tion of ADP-ribosylation factor 6 (ARF6) function during cell invasion. Together, these results suggest that FBX8 is a novel c-Myc binding protein and that c-Myc induces cell invasive activity through the inhibition of FBX8 effects on ARF6 function during cell invasion.

Keywords: c-Myc, cell invasion, FBX8, tumorigenesis, ubiquitination

Mol. Cells
Jan 31, 2023 Vol.46 No.1, pp. 1~67
COVER PICTURE
RNAs form diverse shapes and play multiple functions as central molecules of gene expression. In this special issue on RNA, seven minireviews illustrate how basic concepts and recent RNA biology findings are transformed into new and exciting RNA therapeutics.

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