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Lack of modulatory function of coding nucleotide polymorphism S100A2_185G>A in oral squamous cell carcinoma
Author(s) -
Tsai WC,
Lin YC,
Tsai ST,
Shen WH,
Chao TL,
Lee SL,
Wu LW
Publication year - 2011
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2010.01738.x
Subject(s) - allele , biology , coding region , heterozygote advantage , microbiology and biotechnology , gene , genetics , cancer research , epidermoid carcinoma , cancer
Oral Diseases (2011) 17 , 283–290 Objective: S100A2, a Ca 2+ ‐binding protein with two EF‐hands, is a tumor suppressor in oral cancer. Helix III flanking the C‐terminal EF‐hand is implicated to participate in the interaction of S100A2 and its target(s). The aim of this study was to examine if the coding sequence polymorphism S100A2_185G>A, leading to the peptide 62 substitution of asparagine (AAC, A allele) for serine (AGC, G allele) in helix III, had modulation effects on S100A‐mediated tumor suppression. Subjects and Methods: We sequenced the coding sequence of S100A2 gene in normal oral keratinocytes (NOKs), dysplastic oral keratinocytes (DOKs), eight oral cancer lines, and 54 pairwise oral cancer specimens. We also compared the in vitro anti‐tumor effect of wildtype (G allele) and variant (A allele) S100A2 expression using cell proliferation, migration, invasion, and colony formation assays. Results: With the exception of CAL27 and SCC‐15 cancer lines being heterozygotes of A and G alleles, the remaining oral cells were homozygotic in G alleles. No alterations of anti‐growth, anti‐migration, anti‐invasion, and anti‐colony formation were observed between variant and wildtype cells. Moreover, no minor S100A2_185A allele was detected in 54‐pairwise clinical specimens. Conclusion: The coding sequence polymorphism S100A2_185G>A had no regulatory role in S100A2‐mediated tumor suppression in oral cancer.