Dr. Rafiq Zakaria Campus, Y. B. Chavan College of Pharmacy, Aurangabad, 431001, Maharashtra, India.
Department of Pharmaceutical Chemistry, Rajarshi Shahu College of Pharmacy, Buldana, Maharashtra, India.
Naunyn Schmiedebergs Arch Pharmacol. 2024 Aug;397(8):6107-6119. doi: 10.1007/s00210-024-03021-x. Epub 2024 Feb 28.
The present study aimed to investigate the anti-cancer mechanism of canagliflozin (CANA) and dapagliflozin (DAPA), sodium-glucose co-transporter-2 (SGLT2) inhibitors, using in silico and in vitro approaches. Network pharmacology was employed to predict the targets of the inhibitors and GO gene enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation conducted to explore the interacting pathways. Molecular docking and molecular dynamic (MD) simulation studies were performed to confirm the important targets and assess conformational stability. In vitro cytotoxicity assays, MIA-PaCa-2 and DU-145 cell lines CANA and DAPA was performed. Protein-protein interaction (PPI) network analysis indicated that CANA and DAPA exert anticancer effects through MAPK, mTOR, EGFR-KRAS-BRAF, FGFR, and PI3KA pathways. KEGG analysis revealed that these inhibitors could be used in the treatment of various cancers, including breast, prostate, pancreatic, chronic myeloid leukemia, thyroid, small cell lung, gastric, and bladder cancer. Docking results showed highest affinity for MAPK1 for CANA (- 9.60 kcal/mol) and DAPA (- 9.58 kcal/mol). MD simulation results showed that RMSD values for the MAPK1-compound exhibit remarkable stability over a timeframe of 100 ns. In cytotoxicity assays using MIA-PaCa-2 and DU-145 cell lines, CANA demonstrated a potential antiproliferative effect on the pancreatic cell line MIA-PaCa-2 after 48 h of treatment at a concentration of 100 µg/ml. Furthermore, CANA arrested the cell cycle in the sub-G1 phase and induced late apoptosis and necrosis in MIA-PaCa-2 cell line. Based on these findings, CANA shows promise as a potential novel treatment strategy for pancreatic cancer.
本研究旨在通过计算机模拟和体外实验方法研究坎格列净(CANA)和达格列净(DAPA),即钠-葡萄糖协同转运蛋白 2(SGLT2)抑制剂的抗癌机制。采用网络药理学预测抑制剂的靶点,并进行 GO 基因富集分析和京都基因与基因组百科全书(KEGG)通路注释,以探讨相互作用的通路。进行分子对接和分子动力学(MD)模拟研究,以确认重要靶点并评估构象稳定性。在体外进行了细胞毒性测定,使用 MIA-PaCa-2 和 DU-145 细胞系,研究了 CANA 和 DAPA 的作用。蛋白质-蛋白质相互作用(PPI)网络分析表明,CANA 和 DAPA 通过 MAPK、mTOR、EGFR-KRAS-BRAF、FGFR 和 PI3KA 通路发挥抗癌作用。KEGG 分析表明,这些抑制剂可用于治疗各种癌症,包括乳腺癌、前列腺癌、胰腺癌、慢性髓性白血病、甲状腺癌、小细胞肺癌、胃癌和膀胱癌。对接结果显示,CANA 和 DAPA 对 MAPK1 的亲和力最高,CANA(-9.60 kcal/mol)和 DAPA(-9.58 kcal/mol)。MD 模拟结果表明,在 100 ns 的时间范围内,MAPK1-化合物的 RMSD 值表现出显著的稳定性。在使用 MIA-PaCa-2 和 DU-145 细胞系的细胞毒性测定中,CANA 在浓度为 100 µg/ml 时,对胰腺细胞系 MIA-PaCa-2 表现出潜在的抗增殖作用,作用 48 小时后。此外,CANA 使 MIA-PaCa-2 细胞周期停滞在 sub-G1 期,并诱导晚期细胞凋亡和坏死。基于这些发现,CANA 有望成为治疗胰腺癌的一种新的潜在治疗策略。