این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۸، شماره ۱، صفحات ۱۱۳-۱۲۰
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Plinabulin exerts an anti-proliferative effect via the PI3K/AKT/mTOR signaling pathways in glioblastoma
چکیده انگلیسی مقاله Objective(s): Plinabulin, a marine-derived anticancer drug targeting microtubules, exhibits anti-cancer effects on glioblastoma cells. However, its therapeutic potential, specifically for glioblastoma treatment, remains underexplored. This study aims to elucidate the mechanisms by which plinabulin exerts its effects on glioblastoma cells.Materials and Methods: Using the SRB and colony formation assay to observe the effect of plinabulin on glioblastoma cell viability. Wound healing and transwell migration assay were used to test the effect of plinabulin on glioblastoma cell metastatic potential. Crucial target genes were identified through RNA sequencing and bioinformatics analysis. Protein levels were evaluated in a concentration-dependent manner using western blot analysis.Results: Plinabulin suppressed glioblastoma cell proliferation by causing cell cycle G2/M phase arrest and inhibited migration. The IC50 values were 22.20 nM in A172 cells and 20.55 nM in T98G cells. Plinabulin reduced AKT and mTOR phosphorylation. Combined with the AKT/mTOR inhibitors LY294002 and rapamycin, plinabulin decreased p-mTOR and EGFR protein levels and increased cleaved-PARP levels. Plinabulin induces autophagy, and using an autophagy inhibitor enhances plinabulin-induced cell apoptosis. This suggests that plinabulin might trigger cytoprotective autophagy in glioblastoma cells. These findings indicate that plinabulin hinders glioblastoma growth and induces protective autophagy via the PI3K/AKT/mTOR pathway. Additionally, plinabulin combined with erlotinib showed greater cytotoxic efficacy than either drug alone in glioblastoma cells in vitro.Conclusion: Our study provides new insights into the efficacy of plinabulin against glioblastoma and highlights the potential clinical utility of combining plinabulin with EGFR inhibitors as a chemotherapy strategy.
کلیدواژه‌های انگلیسی مقاله Akt, Autophagy, EGFR, mTOR, PI3K, PIK3CG, Plinabulin
نویسندگان مقاله | Rouxin Wang
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|School of Medicine, Hangzhou City University, Hangzhou 310015, China


| Jing Cheng
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|School of Medicine, Hangzhou City University, Hangzhou 310015, China


| Huanqi Zhang
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|Department of Clinical Pharmacology, Hangzhou First People’s Hospital, Hangzhou 310006, China


| Kaizhi Luo
School of Medicine, Hangzhou City University, Hangzhou 310015, China|Department of Pharmacy, Zhejiang University of Technology, Hangzhou 310027, China


| Rui Wu
Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou 310015, China


| Yangling Li
Department of Clinical Pharmacology, Hangzhou First People’s Hospital, Hangzhou 310006, China


| Yuanheng Zhu
Department of Pharmacy, Ningbo No.2 Hospital, Ningbo 315010, China


| Chong Zhang
School of Medicine, Hangzhou City University, Hangzhou 310015, China|Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou 310015, China
نشانی اینترنتی https://ijbms.mums.ac.ir/article_25030.html
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات