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Bioorg Chem ; 151: 107681, 2024 Oct.
Article in English | MEDLINE | ID: mdl-39106711

ABSTRACT

Aberrant activation of the Hedgehog (Hh) signalling pathway has been associated with the development and progression of pancreatic cancer. For this reason, blockade of Hh pathway by inhibitors targeting the G protein-coupled receptor Smoothened (SMO) has been considered as a therapeutic target for the treatment of this cancer. In our previous work, we obtained a new SMO ligand based on a purine scaffold (compound I), which showed interesting antitumor activity in several cancer cell lines. In this work, we report the design and synthesis of 17 new purine derivatives, some of which showed high cytotoxic effect on Mia-PaCa-2 (Hh-dependent pancreatic cancer cell lines) and low toxicity on non-neoplastic HEK-293 cells compared with gemcitabine, such as 8f, 8g and 8h (IC50 = 4.56, 4.11 and 3.08 µM, respectively). Two of these purines also showed their ability to bind to SMO through NanoBRET assays (pKi = 5.17 for 8f and 5.01 for 8h), with higher affinities to compound I (pKi = 1.51). In addition, docking studies provided insight the purine substitution pattern is related to the affinity on SMO. Finally, studies of Hh inhibition for selected purines, using a transcriptional functional assay based on luciferase activity in NIH3T3 Shh-Light II cells, demonstrated that 8g reduced GLI activity with a IC50 = 6.4 µM as well as diminished the expression of Hh target genes in two specific Hh-dependent cell models, Med1 cells and Ptch1-/- mouse embryonic fibroblasts. Therefore, our results provide a platform for the design of SMO ligands that could be potential selective cytotoxic agents for the treatment of pancreatic cancer.


Subject(s)
Antineoplastic Agents , Pancreatic Neoplasms , Purines , Smoothened Receptor , Humans , Smoothened Receptor/antagonists & inhibitors , Smoothened Receptor/metabolism , Purines/chemistry , Purines/pharmacology , Purines/chemical synthesis , Pancreatic Neoplasms/drug therapy , Pancreatic Neoplasms/pathology , Pancreatic Neoplasms/metabolism , Ligands , Antineoplastic Agents/pharmacology , Antineoplastic Agents/chemistry , Antineoplastic Agents/chemical synthesis , Animals , Mice , Structure-Activity Relationship , Drug Screening Assays, Antitumor , Molecular Structure , Cell Proliferation/drug effects , Dose-Response Relationship, Drug , HEK293 Cells , Cell Line, Tumor , NIH 3T3 Cells , Molecular Docking Simulation , Hedgehog Proteins/metabolism , Hedgehog Proteins/antagonists & inhibitors
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