IADR Abstract Archives
Adipocytes Stimulate Tumour Cell Motility Though Secreted Factors Including Adipokines
Objectives: Oral squamous cell carcinoma (OSCC) displays high rates of metastasis to cervical lymph nodes. The mechanism of this local spread is poorly understood; in particular the role of the interaction between malignant cells and stromal adipocytes in the tumour microenvironment (TME). Adipocytes can act as a source of energy for tumour cells and also represent a reservoir of chemical signals such as adipocytokines.
The present study aims to investigate whether adipocytes can influence oral cancer cell growth and motility in vitro.
Methods: The effect of adipocyte conditioned media (ACM) from differentiated mouse 3T3-L1 cells, and the most abundant secreted adipocytokines, adiponectin (APN) and leptin (LEP), on oral cancer cell (H357 and SCC9) proliferation and migration was assessed using MTS proliferation and Transwell migration assays. The presence of adipocyte ligands and their receptors on the selected OSCC cell lines and oral cancer tissue sections was assessed using flow cytometry and immunohistochemistry.
Results: Our results show that neither ACM or adipokines (up to 100 µg/ml) significantly influenced OSCC cell proliferation. However, ACM increased cell migration (cells/field) in H357 and SCC9 cell lines by 15 and 16 fold respectively compared to the media negative control (contr., p<0.0001, n=3 for all comparisons). Adiponectin (1mg/ml) increased cell migration in H357 and SCC9 cell lines by 9 and 5 fold respectively (p<0.0095 & p<0.0446) and leptin by 7 and 5 fold respectively (p<0.0001 & p<0.0446). FACS results show that APN and LEP receptors are widely expressed on the surface of the selected cell lines. IHC results reveal a high expression of LEP receptors, while there was no expression of APN receptors on the selected OSCC tissue sections.
Conclusions: Adipocytes may therefore influence tumour cell motility by secreting factors including adipocytokines. Further investigations will examine the expression of other adipocytokines in different histological grades of oral cancer tissue and metastatic lymph nodes. Adipocytes will also be co-cultured with OSCC cell lines to mimic the TME and model the interaction between adipocytes and tumour cells.
The present study aims to investigate whether adipocytes can influence oral cancer cell growth and motility in vitro.
Methods: The effect of adipocyte conditioned media (ACM) from differentiated mouse 3T3-L1 cells, and the most abundant secreted adipocytokines, adiponectin (APN) and leptin (LEP), on oral cancer cell (H357 and SCC9) proliferation and migration was assessed using MTS proliferation and Transwell migration assays. The presence of adipocyte ligands and their receptors on the selected OSCC cell lines and oral cancer tissue sections was assessed using flow cytometry and immunohistochemistry.
Results: Our results show that neither ACM or adipokines (up to 100 µg/ml) significantly influenced OSCC cell proliferation. However, ACM increased cell migration (cells/field) in H357 and SCC9 cell lines by 15 and 16 fold respectively compared to the media negative control (contr., p<0.0001, n=3 for all comparisons). Adiponectin (1mg/ml) increased cell migration in H357 and SCC9 cell lines by 9 and 5 fold respectively (p<0.0095 & p<0.0446) and leptin by 7 and 5 fold respectively (p<0.0001 & p<0.0446). FACS results show that APN and LEP receptors are widely expressed on the surface of the selected cell lines. IHC results reveal a high expression of LEP receptors, while there was no expression of APN receptors on the selected OSCC tissue sections.
Conclusions: Adipocytes may therefore influence tumour cell motility by secreting factors including adipocytokines. Further investigations will examine the expression of other adipocytokines in different histological grades of oral cancer tissue and metastatic lymph nodes. Adipocytes will also be co-cultured with OSCC cell lines to mimic the TME and model the interaction between adipocytes and tumour cells.