Volume 37, Issue 2 pp. 97-106

Proteomics-based Identification of Proteins with Altered Expression Induced by 12-O-Tetradecanoylphorbol 13-acetate in Nasopharyngeal Carcinoma CNE2 Cells

Pei-Zhou JIANG

Pei-Zhou JIANG

Cancer Research Institute, Southern Medical University, Guangzhou 510515, China;

Department of Histology and Embryology, Southern Medical University, Guangzhou 510515, China;

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Ming GAN

Ming GAN

Department of Parasitology, Zhongshan Medical College, SUN Yat-sen University, Guangzhou 510080, China

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Hua HUANG

Hua HUANG

Cancer Research Institute, Southern Medical University, Guangzhou 510515, China;

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Xin-Ming SHEN

Xin-Ming SHEN

Cancer Research Institute, Southern Medical University, Guangzhou 510515, China;

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Shuang WANG

Shuang WANG

Cancer Research Institute, Southern Medical University, Guangzhou 510515, China;

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Kai-Tai YAO

Corresponding Author

Kai-Tai YAO

Cancer Research Institute, Southern Medical University, Guangzhou 510515, China;

*Corresponding author: Tel/Fax, 86-20-61648225; Fax, 86-20-61648225; E-mail, [email protected]Search for more papers by this author
First published: 09 February 2005
Citations: 5

Abstract

Abstract Nasopharyngeal carcinoma (NPC) is a malignancy with high incidence in Southern China and South-East Asia. Etiology studies indicate that chemical carcinogen promoters, such as 12-Otetradecanoylphorbol-13-acetate (TPA), are important factors causing NPC development. However, the mechanism of the TPA effect on NPC remains unclear. In the present study, cells from a poorly differentiated squamous cell carcinoma NPC cell line, CNE2, were stimulated by TPA and proteomics technology was carried out to find protein discrepancies between control and TPA-treated cells. Results revealed that TPA treatment in CNE2 cells could upregulate the expression of “triosephosphate isomerase” and “14-3-3 protein sigma” and downregulate the expression of “reticulocalbin 1 precursor”, “nucleophosmin”, “mitochondrial matrix protein p1 precursor”, and “stathmin”. The changes in the expression of these genes suggested that TPA induced CNE2 cells to antiproliferation and to apoptosis, which was confirmed by subsequent apoptosis detection. Therefore, the effects of TPA on nasopharyngeal carcinoma cells were distinct from the effects on primary epithelial cells and we suggest reasons for these differences.

Edited by Rong ZENG

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