Type 2 Diabetes, Obesity, and Cancer Share Some Common and Critical Pathways

Abstract

Diabetes and cancer are among the most frequent and complex diseases. Epidemiological evidence showed that the patients suffering from diabetes are significantly at higher risk for a number of cancer types. There are a number of evidence that support the hypothesis that these diseases are interlinked, and obesity may aggravate the risk(s) of type 2 diabetes and cancer. Multi-level unwanted alterations such as (epi-)genetic alterations, changes at the transcriptional level, and altered signaling pathways (receptor, cytoplasmic, and nuclear level) are the major source which promotes a number of complex diseases and such heterogeneous level of complexities are considered as the major barrier in the development of therapeutic agents. With so many known challenges, it is critical to understand the relationships and the commonly shared causes between type 2 diabetes and cancer, which is difficult to unravel and understand. Furthermore, the real complexity arises from contended corroborations that specific drug(s) (individually or in combination) during the treatment of type 2 diabetes may increase or decrease the cancer risk or affect cancer prognosis. In this review article, we have presented the recent and most updated evidence from the studies where the origin, biological background, the correlation between them have been presented or proved. Furthermore, we have summarized the methodological challenges and tasks that are frequently encountered. We have also outlined the physiological links between type 2 diabetes and cancers. Finally, we have presented and summarized the outline of the hallmarks for both these diseases, diabetes and cancer.

Keywords: breast cancer; cancer; ovarian cancer; shared genes and proteins; type 2 diabetes.

Figure 1

A diagram representing the association between cancer, diabetes, and obesity, followed by shared markers.

Figure 2

The basic mechanism of type 2 diabetes. Here, we have shown the well-established mechanism of how T2D arise in case of human, which mainly focus on beta-cell anomaly, insulin resistance, and IAPP formation.

Figure 3

Hallmarks of diabetes and cancer. Representing the major affected biological processes, pathways, and mechanisms.

Figure 4

A detailed representation of PI3K–AKT pathways with the list of known interactor partners that appear to be a major link (in terms of common cause and therapeutic targets) between cancer and diabetes.

Figure 5

Common links or genes and pathways are based on the analysis of freely available gene expression datasets. Here, we have clearly presented a network of commonly differentially expressed and commonly enriched pathways in case of diabetes as well as one type of cancer, i.e., breast cancer.