acy-1215 has been researched along with Brain-Neoplasms* in 2 studies
2 other study(ies) available for acy-1215 and Brain-Neoplasms
| Article | Year |
|---|---|
Discovery of HDAC6-Selective Inhibitor NN-390 with
Histone deacetylase 6 (HDAC6) has been targeted in clinical studies for anticancer effects due to its role in oncogenic transformation and metastasis. Through a second-generation structure-activity relationship (SAR) study, the design, and biological evaluation of the selective HDAC6 inhibitor Topics: Antineoplastic Agents; Brain Neoplasms; Cell Line, Tumor; Cell Survival; Computer Simulation; Drug Discovery; Drug Screening Assays, Antitumor; Histone Deacetylase 6; Histone Deacetylase Inhibitors; Humans; Medulloblastoma; Models, Molecular; Molecular Docking Simulation; Neoplastic Stem Cells; Structure-Activity Relationship | 2022 |
Temozolomide-resistant Glioblastoma Depends on HDAC6 Activity Through Regulation of DNA Mismatch Repair.
Histone deacetylase 6 (HDAC6) is considered as one of the most promising targets in drug development for cancer therapy. Drug resistance is a major cause of treatment failure in many cancers including glioblastoma (GBM), the most lethal malignant tumor. The role of HDAC6 in GBM resistance and its underlying mechanisms have not been well elucidated. Herein, we investigated the function of HDAC6 in modulating GBM resistance.. The anticancer effects of four structurally distinct selective HDAC6 inhibitors were addressed using western blot, flow cytometry, CCK-8 assay, and CI in temozolomide (TMZ)-resistant GBM cells.. We showed that HDAC6-selecitve inhibitors block activation of the EGFR and p53 pathways in TMZ-resistant GBM cells. Importantly, the inhibition of HDAC6 correlates with increased levels of MSH2 and MSH6, key DNA mismatch repair proteins, in TMZ-resistant GBM cells. In addition to the MSH, HDAC6 inhibitors decrease MGMT expression in TMZ-resistant GBM cells. Furthermore, HDAC6 inhibitors increase TMZ sensitivity and efficiently induce apoptosis in TMZ-resistant GBM cells.. Selective inhibition of HDAC6 may be a promising strategy for the treatment of TMZ-resistant GBM. Topics: Antineoplastic Agents, Alkylating; Benzene Derivatives; Brain Neoplasms; Cell Line, Tumor; Cell Survival; DNA Mismatch Repair; DNA Modification Methylases; DNA Repair Enzymes; DNA-Binding Proteins; Drug Resistance, Neoplasm; ErbB Receptors; Glioblastoma; Histone Deacetylase 6; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; Indoles; MutS Homolog 2 Protein; Pyrimidines; Temozolomide; Tumor Suppressor Protein p53; Tumor Suppressor Proteins; Up-Regulation | 2019 |