Inhibition of LONP1 Suppresses Pancreatic Cancer Progression Via c-Jun N-Terminal Kinase Pathway–Meditated Epithelial-Mesenchymal Transition. Issue 5 (May 2019)

• Record Type: Journal Article
• Authors: Liu, Can; Wang, Hai; Li, Hao; Chen, Xiong; Wu, Xiang; Lu, Bin; Zhang, Wenling; Zhou, Yong; Xiao, Gary Guishan; Gao, Ge
• Is Part Of: Pancreas. Volume 48:Issue 5(2019)
• Publication Date: 2019-05
• Subjects: pancreatic cancer -- LONP1 -- EMT -- JNK -- MMP2 -- MMP9; Pancreas -- Diseases -- Periodicals; Pancreas -- Periodicals; Neuroendocrine tumors -- Periodicals; 616.37005
• DOI: 10.1097/MPA.0000000000001321
• Languages: English
• ISSNs: 0885-3177

Abstract

Abstract : Objective: The aim of this study was to investigate the role of LONP1 in the progression of pancreatic cancer. Methods: Lentivirus was used to silence LONP1 in PANC-1 cells. Colony formation assay, cell counting kit (CCK8) assay, cell scratch-wound assay, and transwell assay were used to assess the effects of our strategy on inhibiting cancer growth, migration, and invasion. Protein expression was detected by Western blot analysis. Results: The expression of LONP1 in pancreatic carcinoma tissues was higher than that in adjacent normal pancreatic tissues. Downregulation of LONP1 suppressed the proliferation, migration, and invasion of PANC-1 cells. Knockdown of LONP1 in PANC-1 cells inhibited epithelial-mesenchymal transition and matrix metalloprotein (MMP) 2/9 by downregulation of vimentin, snail, slug, MMP2, and MMP9 and upregulation of claudin-1. The c-Jun N-terminal kinase pathway was inactivated in LONP1 knockdown PANC-1 cells. Activation of the c-Jun N-terminal kinase pathway by anisomycin treatment significantly reversed the changes in epithelial-mesenchymal transition markers and MMP2/9 induced by ablation of LONP1 in PANC-1 cells. Conclusions: LONP1 plays a vital role in the proliferation and metastasis of pancreatic cancer, which provides a potential therapeutic target for the treatment of pancreatic cancer.