Open AccessUn-methylation of the survivin gene has no effect on immunohistochemical expression of survivin protein in lung cancer patients with squamous cell carcinoma
Author(s) -
Ömer Yalçın,
Metin Budak
Publication year - 2017
Publication title -
bratislavské lekárske listy/bratislava medical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.387
H-Index - 32
eISSN - 1336-0345
pISSN - 0006-9248
DOI - 10.4149/bll_2017_032
Subject(s) - survivin , cancer research , methylation , dna methylation , biology , immunohistochemistry , lung cancer , apoptosis , bisulfite sequencing , exon , microbiology and biotechnology , inhibitor of apoptosis , programmed cell death , gene expression , gene , pathology , medicine , immunology , genetics
Survivin is a member of the inhibitor of apoptosis (IAP) family. The function of the survivin protein is to inhibit caspase activation, thereby leading to negative regulation of apoptosis or programmed cell death. This has been shown by the disruption of survivin induction pathways leading to an increased apoptosis and decreased tumour growth. These data suggest that survivin may provide a new target for cancer treatment, which would distinguish transformed cells from normal cells. In the present study, we aimed to investigate exon 1 of the survivin gene by means of methylation-specific PCR and evaluate its impact on survivin protein expression following DNA isolation and bisulphite modification in paraffin-embedded normal and tumour tissues of lung cancer patients with squamous cell carcinoma. We used 41 squamous cancer tissues with methylation in exon 1 of the survivin gene and non-methylation in corresponding tumours. However, the immunohistochemistry staining of these samples demonstrated an increased survivin protein compared to normal tissue. While there is almost no other study to date on this subject matter, we believe that the absence of methylation in exon 1 of the survivin gene may not affect disease prognosis as it has no effect on expression, and possible promoter methylation or transcription factors (Tab. 1, Fig. 4, Ref. 15).