MNT inhibits the migration of human hepatocellular carcinoma SMMC7721 cells

Journal Article · Fri Feb 03 00:00:00 EST 2012 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2011.12.140· OSTI ID:22207682

Wu, Jian ^[1]; Zhou, Qi ^[1]; Wang, Yafeng; Zhou, Xiangbing ^[1]; Li, Jiaping ^[2]

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1. Department of Hepatobiliary Surgery, The First Affiliated Hospital, Sun Yat-sen University, 58 ZhongShan 2nd Road, Guangzhou, Guangdong 510080 (China)
2. Department of Interventional Oncology, The First Affiliated Hospital, Sun Yat-sen University, 58 ZhongShan 2nd Road, Guangzhou, Guangdong 510080 (China)

Highlights: Black-Right-Pointing-Pointer MNT is a member of the Myc/Max/Mad network that plays a role in cell proliferation. Black-Right-Pointing-Pointer Our study further emphasized the role of MNT in migration inhibition of SMMC7721 cells. Black-Right-Pointing-Pointer MNT might be a promising target for HCC chemotherapy. -- Abstract: Max binding protein (MNT) is a member of the Myc/Max/Mad network that plays a role in cell proliferation, differentiation and apoptosis. We previously observed that MNT was differentially expressed in hepatocellular carcinoma (HCC) and interacted with Nck1 by 2-DE. Nck family adaptor proteins function to couple tyrosine phosphorylation signals, regulate actin cytoskeletal reorganization and lead to cell motility. In order to investigate the regulatory role of MNT in HCC migration, we used transient transfection with a MNT expressing vector to overexpress MNT protein in SMMC7721 cells, and MNT siRNA to knockdown MNT expression. Rho Family Small GTPase activation assay, Western blots and transwell assay were used to determine the migration potential of cells. We found that knockdown of MNT expression might promote SMMC7721 cell migration, while the overexpressed MNT could significantly inhibit cell migration. It further emphasized the role of MNT in inhibition of cell migration that might be a promising target for HCC chemotherapy.

• OSTI ID: 22207682
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 418, Issue 1; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ACTIN
APOPTOSIS
CELL PROLIFERATION
CHEMOTHERAPY
HEPATOMAS
INHIBITION
PHOSPHORYLATION
TYROSINE