Low glucose availability alters the expression of genes involved in initial adhesion of human glioblastoma cancer cell line SF767

Studying the metabolic pathways of cancer cells is considered as a key to control cancer malignancies and open windows for effective drug discovery against cancer. Of all the properties of a tumor, metastasis potential is a defining characteristic. Metastasis is controlled by a variety of factors that directly control the expression of cell adhesion proteins. In this study we have investigated the expression of cell to cell and cell to matrix adhesion protein genes during the initial phases of attachment of human glioblastoma cancer cell line SF767 (66Y old human female: UCSF Neurosurgery Tissue Bank) to the attachment surface under (Cell culture treated polystyrene plate bottom) glucose‐rich and glucose‐starved conditions. The aim was to imitate the natural microenvironment of glucose availability to cancer cells inside a tumor that triggers epithelial to mesenchymal transition (EMT). In this study, we have observed the gene expression of epithelial and mesenchymal isoforms of cadherin (E‐CAD and N‐CAD) and Ig like cell adhesion molecules (E‐CAM and N‐CAM) along with Integrin family subunits for the initial attachment of cancer cells. We observed that high glucose environments promoted cell survival and cell adhesion, whereas low glucose accelerated EMT by downregulating the expression level of integrin, E‐CAD, and N‐CAD, and upregulation of N‐CAM during early period of cell adhesion. Low glucose availability also downregulated variety of structural and regulatory genes, such as zinc finger E‐box binding home box 1A), cytokeratin, Snail, and β catenin, and upregulation of hypoxia‐inducible factor 1, matrix metalloprotease 13/Collagenase 3, vimentim, p120, and fructose 1,6 bisphosphatase. Glucose conditions are more efficient for cancer studies in this case glioblastoma cells. High glucose environments promote cell survival and cell adhesion, whereas low glucose accelerates EMT by downregulating the level of integrin, E‐CAD, and N‐CAD, and upregulation of N‐CAM. Low glucose availability also downregulated a variety of structural and regulatory genes such as ZEB1A, CTK, Snail, and BCT and upregulation of HIF1, MMP13, Vimentin), p120 and Fructose 1,6 bisphosphatase.