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Aberrant expression of serum amyloid A in head and neck squamous cell carcinoma
Author(s) -
Shinriki Satoru,
Ueda Mitsuharu,
Ota Kazutoshi,
Nakamura Masaaki,
Kudo Mareina,
Ibusuki Mutsuko,
Kim Jaemi,
Yoshitake Yoshihiro,
Fukuma Daiki,
Jono Hirofumi,
Kuratsu Junichi,
Shinohara Masanori,
Ando Yukio
Publication year - 2010
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2009.00777.x
Subject(s) - immunohistochemistry , head and neck squamous cell carcinoma , stat3 , stat protein , reverse transcription polymerase chain reaction , cancer research , serum amyloid a , western blot , medicine , pathology , activator (genetics) , head and neck cancer , gene expression , biology , cancer , signal transduction , receptor , inflammation , gene , biochemistry
J Oral Pathol Med (2010) 39 : 41–47 Serum amyloid A (SAA) is an acute‐phase reactant, the blood level of which is often elevated in response to some types of neoplasia. Here, we investigated expression of the gene SAA1 and the protein SAA in head and neck squamous cell carcinoma (HNSCC) and normal oral mucosal tissues as well as blood SAA levels in HNSCC patients. Also, we investigated the effects of inhibiting signal transducer and activator of transcription 3 (STAT3) signaling on SAA1 expression in the HNSCC cell line SAS. Serum SAA levels in HNSCC patients were significantly higher than those in healthy volunteers. In addition, real‐time quantitative reverse transcription‐polymerase chain reaction analysis revealed a significantly higher SAA1 expression level in HNSCC than in normal mucosa ( P < 0.0001). Furthermore, Western blot and immunohistochemical analyzes revealed that high expression of SAA in carcinomas was detected predominantly in tumor cells, but not in normal mucosal tissues. An inhibitor of STAT3 activation, AG490, significantly reduced SAA1 expression in SAS cells. These data demonstrated that SAA was up‐regulated in HNSCC through the Janus kinase‐STAT3 pathway.