Computer-aided drug design and inhibitive effect of a novel nitrogenous heterocyclic compound and its mechanism on glioma U251 cells and breast cancer MCF-7 cells
Authors Qian L, Zhu Y
Received 14 March 2018
Accepted for publication 1 May 2018
Published 27 June 2018 Volume 2018:12 Pages 1931—1939
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 6
Editor who approved publication: Dr Anastasios Lymperopoulos
Liyu Qian,1 Yu Zhu2
1Department of Tumor Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, China; 2Tianjin Key Laboratory of Cerebral Vessels and Neuraldegenerative Disease, Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin 300350, China
Background: Glioma and breast cancer are severe malignant cancerous tumors that highlight the importance of developing new anti-cancer drugs. The aim of this study was to explore the effects of a novel nitrogenous heterocyclic compound on glioma and breast cancer cells and to determine its mechanism of action.
Methods: We designed and synthesized a novel nitrogenous heterocyclic compound, 3-(4-amino-1H-benzo[d]imidazole-2-carboxamido)-4-oxo-3,4-dihydroimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide, based on alkylglycerone phosphate synthase (AGPS) using computer-aided drug design (CADD), and we measured its effect on the proliferation, invasion, cell cycle and apoptosis of U251 glioma and MCF-7 breast cancer cells. In addition, the compound’s effect on the expression of tumor-related mRNA, circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs) was explored.
Results: It was found that the nitrogenous heterocyclic compound could induce cell cycle arrest at the G2/M phase of U251/MCF-7 cells and activate apoptosis. Real-time PCR showed that the expression levels of tumor-related mRNA, circRNAs and lncRNAs were impacted.
Conclusion: We concluded that the nitrogenous heterocyclic compound inhibits the proliferation and invasion of U251 glioma and MCF-7 breast cancer cells through the induction of apoptosis and cell cycle arrest by regulating tumor-related genes.
Keywords: nitrogenous heterocyclic compound, glioma, breast cancer, proliferation, invasion
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