East Black Sea Journal of Health Sciences, cilt.2, sa.1, ss.45, 2023 (Hakemli Dergi)
Introduction and Aim: Oral squamous cell carcinoma (OSCC) is responsible for more than 91% of
all malignancies in oral cavity. Epigenetic alterations and other environmental factors can cause
changes in gene expression of OSCC pathogenesis. DNA methylation is just one of many epigenetic
alterations. Herein, in our study we focused on predictive biomarker potential of guanine nucleotidebinding protein γ-7 (GNG7) gene methylation. The clinical significance of GNG7 methylation and the
association with oral carcinogenesis is still remain unknown.
Materials and Methods: DNA and RNA samples of tissues and body fluids obtained from OSCC
patients and healthy individuals were used to examine the methylation and expression levels of the
GNG7 gene by using QMSP/QRT-PCR methods, respectively. All results were compared with
clinicopathological and demographical parameters.
Results: GNG7 gene hypermethylation was observed in 18% of patients. It was observed decreased
expression levels in 48% and increased expression levels in 32% OSCC patients. There was a
statistical significance was found between the classification of retromolar trigone with tongue, floor of
the mouth and decreased expression levels. Decreased expression levels of GNG7 gene in tumor,
matched-normal tissues were downregulated in patients than healthy individuals and GNG7 gene
expression levels in patients and healthy individuals’ serum were seen abundant significance.
Conclusion: The GNG7 gene promoter hypermethylation depends on loss of expression in OSCC
patients. The result of loss of expression due to the existence of tumor hypermethylation compared to
healthy people suggests that there is a specific subgroup of OSCC patients for the GNG7 gene in
Turkish population.
Keywords: Oral squamous cell carcinoma; GNG7 gene; Epigenetics; Expression; Methylation
This study was supported by Scientific Research Projects Coordination Unit of Istanbul University (Project
number: IU-BAP-TYL-2019-35412).