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The role of p300 in the tumor progression of oral squamous cell carcinoma
Author(s) -
Cho YoungAh,
Hong JiSoo,
Choe EunJin,
Yoon HyeJung,
Hong SeongDoo,
Lee JaeIl,
Hong SamPyo
Publication year - 2015
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/jop.12227
Subject(s) - immunohistochemistry , biology , exon , dna methylation , epigenetics , cancer research , methylation , tumor suppressor gene , gene , pathology , epidermoid carcinoma , gene expression , cancer , medicine , carcinogenesis , genetics , immunology
Background EP300 gene encoding p300 is a candidate tumor suppressor gene. This study investigated p300 expression and gene alteration in oral squamous cell carcinoma ( OSCC ) specimens to assess its role in OSCC development. Methods Genomic DNA extracted from 13 human OSCC cell lines and 40 OSCC patient specimens was subjected to methylation‐specific PCR and exon sequencing. Immunohistochemical staining with primary antibodies against p300 and p53 was performed in 48 patients with OSCC . We analyzed the association between the data and clinicopathological factors of OSCC patients. Results Methylation‐specific PCR revealed that the EP300 promoter region was not hypermethylated in OSCC . Only one cell line demonstrated a point mutation at exon 31. On immunohistochemical examination, patients with metastatic lymph nodes ( P  =   0.009) and advanced clinical stage ( P  =   0.046) tended to show increased expression of p300. There was no statistically significant relationship between p300 expression and p53 accumulation in OSCC tissue samples. Patient survival was not correlated with p300 expression. Conclusions EP300 is not a tumor suppressor gene because there was neither epigenetic inactivation of the gene nor a mutation resulting in functional impairment. Based on p300 overexpression and its association with clinical factors in patients with OSCC , it is likely that p300 itself or one of its target genes plays a key role in the aggressive phenotypes of OSCC .

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