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Oh, Im, Jung, and Lee: Gene Expression Changes Associated with Sustained p16 Expression in Hepatocellular Carcinoma Cells
Original Article

Immune Network 2004; 4(4): 237-243.

Published online: 31 December 2004

DOI: https://doi.org/10.4110/in.2004.4.4.237

Gene Expression Changes Associated with Sustained p16 Expression in Hepatocellular Carcinoma Cells

Sang-Jin Oh1, Ji-Young Im2, Che-Hun Jung3, Yong-Bok Lee4

1School of Biological Sciences and Technology, Chonnam National University, Gwangju, Korea.

2Department of Biology, Chonnam National University, Gwangju, Korea.

3Department of Chemistry, Chonnam National University, Gwangju, Korea.

4Department of Chemistry, College of Pharmacy, Chonnam National University, Gwangju, Korea.

Corresponding Author (sjo@jnu.ac.kr)

Copyright © 2004 The Korean Association of Immunologists

(open-access):

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background

The normal functions of the cell cycle inhibitor p16INK4a are frequently inactivated in many human cancers. Over 80% of hepatocellular carcinoma (HCC) cases lack a functional p16/Rb pathway. p16/Rb pathway, as well as p53 pathway, is considered as one of key components of tumor suppression.

Methods

To study the roles of p16INK4a in HCC, a stable cell line expressing exogenous p16 was generated from SNU-449 hepatocellular carcinoma cells lacking endogenous p16, and suppression subtractive hybridization (SSH) was performed in parallel with the control cells.

Results

1) SSH identifies fibronectin (FN1), crystallin αB (CRYAB), Rac1, WASP, RhoGEF, and CCT3 as differentially-expressed genes. 2) Among the selected genes, the up-regulation of FN1 and CRYAB was confirmed by Northern blot, RT-PCR and by proteomic methods.

Conclusion

These genes are likely to be associated with the induction of stress fiber and stabilization of cytoskeleton. Further studies are required to clarify the possible role of p16 in the signal transduction pathway.

Keywords: Suppression subtractive hybridization, sustained p16 expression, hepatocellular carcinoma, differential gene expression

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