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Butyrate response factor 1 enhances cisplatin sensitivity in human head and neck squamous cell carcinoma cell lines
Author(s) -
Lee Seung Koo,
Kim Seong Bum,
Kim Jong Soo,
Moon Chang Hoon,
Han Myung Shin,
Lee Byung Ju,
Chung Dae Kyun,
Min Young Joo,
Park Jae Hoo,
Choi Dae Hwa,
Cho Hong Rae,
Park Sang Kyu,
Park Jeong Woo
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.21133
Subject(s) - cisplatin , head and neck squamous cell carcinoma , cancer research , cell culture , apoptosis , cell , gene expression , biology , pathology , medicine , oncology , head and neck cancer , cancer , gene , chemotherapy , biochemistry , genetics
Cisplatin is a widely used chemotherapeutic agent in head and neck squamous cell carcinoma (HNSCC). Resistance to cisplatin is a common feature of HNSCC. To identify genes that may regulate cisplatin sensitivity, we carried out a cDNA microarray analysis of gene expression in cisplatin‐sensitive and cisplatin‐resistant HNSCC‐derived cell lines. Among genes differentially expressed by cisplatin treatment, we have confirmed the elevated expression of butyrate responsive factor 1 ( BRF1 ) in cisplatin‐sensitive HNSCC cells and have demonstrated that the expression level of BRF1 is associated with cisplatin‐sensitivity. Specific inhibition of BRF1 expression using an antisense oligodeoxynucleotide (ODN) decreased the cisplatin‐sensitivity and, on the contrary, overexpression of BRF1 increased cisplatin‐sensitivity in HNSCC cells. Elevated expression of BRF1 decreased the level of the human inhibitor of apoptosis protein‐2 ( cIAP2 ) and increased the caspase‐3 activity in HNSCC cells. In addition, elevated expression of BRF1 decreased the expression level of enhanced green fluorescent protein (EGFP) linked to a 3′ terminal AU‐rich element (ARE) of cIAP2 mRNA. These findings demonstrate that BRF1 expression enhanced cisplatin sensitivity in HNSCC cells by reducing the levels of cIAP2 mRNA. © 2005 Wiley‐Liss, Inc.