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| Crebanine inhibits pancreatic cancer cell growth through DUSP5/ERK signaling pathway |
| LIN Chengyin1,XIANG Shixuan2, CHEN Letaotao3, DENG Jie4. |
| 1.The First School of Medicine, School of Information and Engineering, Wenzhou Medical University, Wenzhou 325035, China; 2.Alberta Institute, Wenzhou Medical University, Wenzhou 325035, China; 3.Renji College, Wenzhou Medical University, Wenzhou 325035, China;4.Zhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, China |
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| Cite this article: |
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LIN Chengyin,XIANG Shixuan,CHEN Letaotao, et al. Crebanine inhibits pancreatic cancer cell growth through DUSP5/ERK signaling pathway[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2024, 54(8): 623-630.
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Abstract Objective: To explore the effect of crebanine on the proliferation and apoptosis of pancreatic cancer cells and its potential mechanism. Methods: CCK8, clone formation assay and EdU staining were used
to detect the effect of crebanine on the proliferation of human pancreatic cancer cells Panc-1 and Patu-8988. The effect of crebanine on apoptosis was detected by flow cytometry and TUNEL staining. Western blot assay was conducted to determine the effects of crebanine on DUSP5 protein, proliferation-related protein Ki67, apoptosisrelated proteins Bcl-2 and Bax, and p-ERK1/2. Results: After 24 h treatment with crebanine, the proliferation ability of pancreatic cancer cells decreased (P<0.05), while the apoptosis rate increased significantly (P<0.05).Meanwhile, the expression of DUSP5 was markedly upregulated (P<0.05), and the expression of p-ERK1/2 was downregulated (P<0.05). Knockdown of DUSP5 effectively reversed the anti-proliferation and pro-apoptotic abilities of crebanine in pancreatic cancer cells (all P<0.05), and partially restored the p-ERK1/2 protein reduced by crebanine (P<0.05). Conclusion: Crebanine inhibits the proliferation and promotes apoptosis of pancreatic cancer cells by upregulating DUSP5 expression and subsequently inactivating ERK1/2 signaling.
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Received: 15 March 2024
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