Potential Biomarkers for Early Detection of Oral Cancer: Leptin and Adiponectin
Project no. 413 · Status: Kapanmış · 2018
Summary
Aim: Adipokines are bioactive proteins that regulate metabolism, inflammation, angiogenesis and proliferation. In studies which evaluate the relationship between leptin and adiponectin, with the development of cancer, it was suggested that there may be a positive relationship between the increase in serum leptin level and tumor growth, and adiponectin can suppress development of cancer. However, contradictory results have also been reported making the role of adipokines in cancer development still questionable. The aim of this study is to determine adiponectin and leptin expression levels in tissue samples from healthy, dysplastic and cancerous oral lesions, and to investigate the potential role of these biomarkers in oral cancer development. Material and Methods: Paraffine embedded tissue samples from the archives of Ege University, Faculty of Medicine, Department of Pathology which were histologically diagnosed as oral squamous cell carcinoma (OSCC) (n=24), oral dysplasia (n=12) and healthy tissue (n=16) were included in this retrospective study. Total RNA extraction was performed using PureLink FFPE total RNA Isolation kit, and thereafter the concentration and purity of samples were determined with NanodropTM device (Thermo Scientific). Complementary DNA synthesis from isolated RNA was performed using High-Capacity cDNA Reverse Transcription kit. The differences between expression levels of leptin and adiponectin in tissues was evaluated with qPCR. Leptin and adiponectin expression levels related to OSCC was performed according to normalizing gene ACTB. ??CT method was used for comparison of leptin and adiponectin expression levels. An increase in expression level was concluded in case the 2-??CT value was over 2, and a decrease in expression level was noted in case the 2-??CT value was under 1. Student t-test was used to compare the differences in gene expression levels between groups, using 2 ^ (- Delta CT) value for each gene. Results: When compared to the healthy group, adiponectin and leptin expression levels were decreased by 1.09 (p = 0.49) and 10.3 (p = 0.22), respectively, in the OSHC group, however the differences were not statistically significant. The level of adiponectin expression decreased 1.65 times (p = 0.62) and the leptin expression increased 3 times (p = 0.30) in the dysplasia group when compared to the healthy group. When the OSHC and dysplasia groups were compared, it was found that the level of adiponectin expression increased 1.52 times (p = 0.99) and the level of leptin expression decreased 30.94 times (p = 0.16) in the OSHC group. The samples were re-grouped as increased risk (OSCC+dysplasia) (n=36) and healthy (n=16) and a decrease by 16.5 (p= 0.3) in leptin expression and an increase by 1.14 (p= 0.6) in adiponectin expression was observed in increased risk group compared to the healthy group. Conclusion: The expression levels for leptin and adiponectin in tissue samples from oral lesions diagnosed as healthy, dysplastic and OSCC has not been compared before. An increase in serum leptin level in oral premalignant lesions and a decrease in serum adiponectin levels in tongue cancer was reported previously. The results of the present study revealed a significant decrease in leptin expression and an increase in adiponectin expression in samples from increased risk group which included dysplasia and OSCC tissue samples. Further studies with larger study samples are needed to clarify the roles of leptin and adiponectin in oral cancer development.