TSC22D1 in pancreatic beta cells and C-MYC in cancer cells: Exploring therapeutic targets for diabetes and cancer

Since diabetes mellitus and cancer are among the world's major causes of illness and mortality, new treatment approaches are desperately needed. The control of pancreatic beta cell activity and the creation of designed cancer treatments are two different but related fields of molecular biology that are examined in this work. In the first part of the study, we identify TSC22D1 as a novel pancreatic beta cell function regulator. Using INS-1E cells, we demonstrate that TSC22D1 depletion enhances the expression of key beta cell identity genes such as INS1, INS2, Pdx1, Slc2a2, and Nkx6.1 while promoting glucose-stimulated insulin secretion without affecting intracellular insulin content. Mechanistically, we uncover a reciprocal interaction between TSC22D1 and FoxO1, which regulate glucose-responsive processes including mRNA processing, ribonucleoprotein complex biogenesis, and Golgi vesicle transport. These findings highlight TSC22D1 as a pivotal regulator of beta cell function with potential implications for diabetes treatment. The second part of the study focuses on the development of novel small-molecule inhibitors targeting the c-Myc/Max complex, a critical driver of tumourigenesis. A library of c-Myc inhibitors was screened across several cancer cell lines, including PANC1, MCF7, DU145, and A549. Among these, the inhibitor c-Myc-i7 exhibited remarkable anticancer potency, with IC50 values as low as 1.6 μM and up to 40 times greater efficacy than reference compounds. Notably, c-Myc-i7 demonstrated exceptional selectivity, showing a 37-fold and 59-fold preference for targeting prostate and breast cancer cells over healthy cells, respectively. Together, these discoveries point to the therapeutic potential of c-Myc inhibitors in cancer treatment and provide important new insights into the molecular control of beta cell activity, opening the door to new cancer and diabetes treatments.