Dataset: Expression analysis of the glucose deprivation-induced human tumor cell responses

The tumor microenvironment is characterized by low glucose and hypoxia. It is well known that changes in the tumor microenvironment, such as hypoxia and low glucose, can increase the production of VEGF. Although the role of hypoxia in the regulation of VEGF production is well understood, the mechanism linking glucose deprivation (GD) to tumor growth and angiogenesis is unclear. Here, GD (a physiological stimulus) was used to treat human tumor cells. The transcriptional reprogramming of tumor cells by GD was measured with microarray technology to provide a comprehensive analysis of the gene expression profile underlying the GD treatment. Our study suggested that GD initiates an angiogenic switch by increasing the expression of proangiogenic mediators (VEGF, FGF2, IL6, etc.) and decreasing the expression of angiogenesis inhibitors (THBS1, CXCL14 and CXCL10). The markers of Unfolded Protein Response (UPR) (Grp78/Bip, CHOP, ATF4, etc.) were significantly increased. The above results suggest GD may regulate angiogenesis through activation of the UPR. UM-SCC-81B cells (human oral squamous cell carcinoma cell line) were treated with glucose deprivation (GD) for 4 hours (UM-SCC-81B-GD-4) and 24 hours (UM-SCC-81B-GD24). Cells without treatment were used as a non-treatment control (UM-SCC-81B-NT). Each sample was analyzed once, i.e., without biological replicates. The expression of the genes of interest was confirmed with real-time PCR, ELISA and Western blot.

Species:

human

Samples:

3

Source:

E-GEOD-38583

PubMed:

22915762

Updated:

Dec.12, 2014

Registered:

Sep.19, 2014