Research shows that metformin has an unclear relationship with cancer cell composition. According to Pircher et al. (2018), diabetic patients and non-diabetic patients with cancer indicate some significant differences in tumor composition and activity. In a study of 167 patients with both diabetes mellitus and prostate cancer, Pircher et al. (2018), could not find any link between the cancer progression and antidiabetic drugs. However, immunohistochemistry revealed that cancer patients with diabetes mellitus had decreased mTOR activation. Specifically, the results were visible in patients using metformin and insulin. The researchers concluded that diabetes drugs have some effect on tumor biology. The researchers found different tumor biology in patients with antidiabetic medications compared to those without it. However, the study did not put into consideration the length of diabetes drug use. The study also investigated a small group of patients. The study was a controlled study that examined a group of cancer patients with diabetes drugs against a control group without the condition. In a similar control study, Feng et al. (2015), could not find any link between metformin and prostate cancer risks. The researchers could not find any significant association between non-metformin drugs with prostate cancer risks.

However, in a review of preclinical and clinical data regarding the topic, researchers found the need for further research on the subject. Shlomai et al. (2016), found that researchers associate specific type 2 diabetes mellitus drugs with cancer. Precisely, researchers associated glucocorticoids with hyperglycemia. They also cause insulin resistance and reduce insulin secretion. Shmolai et al. (2016) also opine that type 2 diabetes patients have lower cases of prostate cancer. However, type two diabetes patients have a high mortality rate concerning other types of cancer. Also, Shmolai et al. (2016) find that insulin has a clear association with tumor growth and metastasis. Insulin may lead to mitogenic signaling in cancers that overexpress IGF-1R. As a result, hyperinsulinemia may lead to tumor growth. These results are similar to earlier research on the same topic. Lin et al. (2015) found that insulin sensitizers can increase prostate cancer progression. Insulin sensitizers inhibit Testicular nuclear Receptor 4 (TR4). By knowing down TR4, the sensitizers increase cell growth in prostate cancer (Lin et al., 2015). This is particularly so when the patient has only one allele TR4 deletion. Cells with wild type TR4 do not show an impact on tumor growth when insulin sensitizers are in use.

However, other researchers have given contradicting evidence on the role of insulin on prostate cancer progression. Haggstrom et al. (2017) found that patients using insulin had a reduced risk of prostate cancer. However, the researchers concluded that there is a relationship between type 2 diabetes mellitus and prostate cancer. Haggstrom et al. (2017) found that longer duration with type 2 diabetes mellitus led to a decreased risk of prostate cancer.  These results tend to support the hypotheses that there is an inverse relationship between prostate cancer and antidiabetic drugs.  However, the results show no clear description of the kind of association and the cause-effect depiction of it. In other words, the researchers have contradicting results on the type of effect that antidiabetic drugs have on cancer patients. Researchers also recommend further research on the topic, citing certain limitations of existing a priori literature. Prior research shows both qualitative and quantitative evidence of the conflicting results on the effects of insulin on prostate cancer tumors and metastasis.

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