Bortezomib inhibits the malignant biological behaviors of pancreatic cancer cells and liver metastasis
10.19405/j.cnki.issn1000-1492.2025.05.008
- VernacularTitle:硼替佐米抑制胰腺癌细胞恶性生物学行为和肝转移
- Author:
Yinfeng Chen
1
;
Xing Huang
2
Author Information
1. Zhejiang University School of Medicine , Hangzhou 310058 ;
2. Zhejiang University School of Medicine , Hangzhou 310058 ; Zhejiang Provincial Key Laboratory of Pancreatic Disease , Hangzhou 310009
- Publication Type:Journal Article
- Keywords:
bortezomib;
pancreatic cancer;
epithelial_mesenchymal transition;
liver metastasis;
migration;
invasion
- From:
Acta Universitatis Medicinalis Anhui
2025;60(5):825-833
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the potential of bortezomib in inhibiting the malignant biological behaviors and liver metastasis of pancreatic cancer cells.
Methods :KPC and Panc02 cell lines were used as a couple of working cells in this study. The CCK-8 assay was used to assess the effect of bortezomib on cell viability in murine pancreatic cancer cells, and the half inhibitory concentration(IC50) values were calculated. The EdU assay was performed to evaluate the impact of bortezomib on the proliferation of these two cell lines. Apoptosis assays were conducted to investigate the pro-apoptotic effects of bortezomib on pancreatic cancer cells. Colony formation, scratch wound healing, and Transwell assays were used to examine the effects of bortezomib on the proliferation, migration, and invasion of pancreatic cancer cells. QRT-PCR and Western blot were employed to assess the impact of bortezomib on the expression of epithelial-mesenchymal transition(EMT) related markers, includingCdh1,Cdh2,VimandSnailgene and E-cadherin protein, N-cadherin protein, Vimentin protein and Snail protein. Anin vivospleen-to-liver metastasis model was established to evaluate the therapeutic value of bortezomib in inhibiting pancreatic cancer liver metastasis.
Results :The CCK-8 assay showed that bortezomib significantly reduced the viability of KPC and Panc02 cells(P<0.000 1), with IC50values of approximately 118.70 nmol/L and 34.16 nmol/L, respectively. The EdU assay showed that bortezomib markedly inhibited the proliferative capacity of pancreatic cancer cells(P<0.01). Apoptosis assays showed that bortezomib promoted both early and late apoptosis in pancreatic cancer cells(P<0.05). Colony formation, scratch wound healing, and Transwell assays showed that bortezomib effectively suppressed colony formation, migration, and invasion(P<0.01) of pancreatic cancer cells. qRT-PCR and Western blot analyses showed that bortezomib altered the expression of EMT-related markers at both the mRNA(the expression level ofCdh1gene increased, while the expression levels ofCdh2,VimandSnailgenes decreased)(P<0.000 1) and protein(the expression level of E-cadherin protein increased, while the expression levels of N-cadherin protein, Vimentin protein and Snail protein decreased) levels in pancreatic cancer cells. Thein vivospleen-to-liver metastasis model demonstrated that bortezomib significantly inhibited pancreatic cancer liver metastasis(P<0.01).
Conclusion:Bortezomib can inhibit the malignant biological behaviors of pancreatic cancer cells, suggesting it might be a potential anti-cancer drug in pancreatic cancer.
- Full text:2026020510354752962硼替佐米抑制胰腺癌细胞恶性生物学行为和肝转移_陈崟峰.pdf
