Dexamethasone And Certain Nonsteroidal Drugs Stimulate The Transcriptional Activity Of GR-In The U2-OS Cancer Cell Line

Abstract

Glucocorticoids are steroid hormones that act as immunosuppressants, immunomodifiers, and anti-inflammatory drugs. A synthetic GC chemical called dexamethasone (Dex) is used for a number of things other than reducing inflammation. Dex stops cell proliferation in leukemia and other cancers. In order to help chemotherapy kill leukemia cells or to minimize side effects from specific chemotherapy drugs, steroids are frequently given along with chemotherapy. The two steroids that are most frequently administered for ALL are prednisolone and dexamethasone. Steroid pills are typically taken. In both people and animals, chronic GC use increases the risk of illnesses in the nephrological system, skeletal system, and metabolism. The current study sought for strategies to improve the current glucocorticoid medication in order to treat leukemia. The effects of numerous substances on cells were examined using a variety of procedures. This study investigated the dissociation effects of CPDA TYRAMINE AND THCL to dexamethasone on wild GR and transfected Mutant GR-I628A using the cancer cell line U2-OS and the luciferase assay. The results show that DEX stimulates the transcriptional activity of wild GR. Following Dex treatment, TAT3 luciferase reporter activity was elevated in both mutant and wild-type GR. The other non-steroidal medications that were tested also demonstrated positive regulation activity, with DEX, T, CpdA, and THCL upregulating TAT3 transcription, in that order. Given that transactivation activity is the only adverse consequence, this implies that other drugs may be less likely to do so than GR.  Additionally, residue I628 appears to be essential for interaction because its mutation decreases GR activity when it interacts with all drugs.