Diabetes mellitus is a burdensome disease that affects various cellular functions through altered glucose metabolism. Several reports have linked diabetes to cancer development; however, the exact molecular mechanism of how diabetes-related traits contribute to cancer progression is not fully understood. The current study aimed to explore the molecular mechanism underlying the potential effect of hyperglycemia combined with hyperinsulinemia on the progression of breast cancer cells. To this end, gene dysregulation induced by the exposure of MCF7 breast cancer cells to hyperglycemia (HG), or a combination of hyperglycemia and hyperinsulinemia (HGI), was analyzed using a microarray gene expression assay. Hyperglycemia combined with hyperinsulinemia induced differential expression of 45 genes (greater than or equal to two-fold), which were not shared by other treatments. On the other hand, in silico analysis performed using a publicly available dataset (GEO: GSE150586) revealed differential upregulation of 15 genes in the breast tumor tissues of diabetic patients with breast cancer when compared with breast cancer patients with no diabetes. SLC26A11, ALDH1A3, MED20, PABPC4 and SCP2 were among the top upregulated genes in both microarray data and the in silico analysis. In conclusion, hyperglycemia combined with hyperinsulinemia caused a likely unique signature that contributes to acquiring more carcinogenic traits. Indeed, these findings might potentially add emphasis on how monitoring diabetes-related metabolic alteration as an adjunct to diabetes therapy is important in improving breast cancer outcomes. However, further detailed studies are required to decipher the role of the highlighted genes, in this study, in the pathogenesis of breast cancer in patients with a different glycemic index.

The incidence of cancer is increasing worldwide as well as in the United Arab Emirates (UAE). Currently, researchers are advocating not only for prevention programs but also for early detection. In this study, we aimed to assess the general awareness of cancer among the UAE population, with a focus on environmental risk factors. A descriptive cross-sectional design was employed, and a structured questionnaire was used to collect data from 385 participants. A total of 91.2% of the study population identified cancer as the leading cause of death, while 64.6% of the subjects were able to identify the key causes of cancer. A total of 87.3% and 70.5% of the participants were able to define tobacco and alcohol, respectively, as cancer-causing agents. Most of the study population failed to identify cancer-related infectious agents and incense smoke as carcinogens. Respondents in the medical professions had the highest knowledge score when compared with respondents with a non-medical profession and unemployed participants (p < 0.0005). To fill the gaps in cancer-related knowledge, participants were asked about their preferred method for cancer education, and 83.9% of the participants favored the media as a source of information. Conclusively, our findings indicated a gap in cancer knowledge among UAE residents, which highlights the importance of educational campaigns by health authorities; a follow-up study evaluating the success of educational campaigns is also warranted.