Identification of Max binding protein as a novel binding protein of Nck1 and characterization of its role in inhibiting human liver cancer SK-HEP-1 cells.
- Author:
Qi ZHOU
1
;
Tao HUANG
;
Ya-feng WANG
;
Kun-sun ZHANG
;
Dong CHEN
;
Bao-gang PENG
Author Information
- Publication Type:Journal Article
- MeSH: Adaptor Proteins, Signal Transducing; genetics; metabolism; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; genetics; metabolism; Blotting, Western; Cell Differentiation; genetics; physiology; Cell Line, Tumor; Cell Movement; genetics; physiology; Humans; Immunoprecipitation; Liver Neoplasms; Oncogene Proteins; genetics; metabolism; Protein Binding; genetics; physiology; Repressor Proteins; genetics; metabolism; Reverse Transcriptase Polymerase Chain Reaction
- From: Chinese Medical Journal 2012;125(18):3336-3339
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDThe tendency of tumor cells to disperse throughout the liver is a distinct feature of hepatocellular carcinoma (HCC). Nck family adaptor proteins function to regulate actin cytoskeletal reorganization that leads to cell motility. We previously found that Max binding protein (MNT) was differentially expressed in HCC, and interacted with Nck1 by 2-DE. MNT is a protein member of the Myc/Max/Mad network which plays roles in cell proliferation, differentiation, and death. We investigated the effects of MNT on migration of human liver cancer SK-HEP-1 cells to study the migration regulatory role of MNT in HCC cells.
METHODSInteraction between MNT and Nck1 was further validated in hepatoma cells by GST-pull down assay and immunoprecipitation. siRNAs specific to MNT (MNT siRNA) were used to knockdown MNT expression. Western blotting, transwell assay were used to determine the migration potential of cells.
RESULTSInteraction between MNT and Nck1 was validated in hepatoma cells. MNT knockdown promoted the migration of human liver cancer SK-HEP-1 cells (P < 0.01).
CONCLUSIONThe results suggest that MNT, via interaction with Nck1, inhibits hepatoma cell migration.
