Antibiotic tigecycline inhibits cell proliferation, migration and invasion via down‐regulating CCNE2 in pancreatic ductal adenocarcinoma

Abstract

Recently, many researches have reported that antibiotic tigecycline has significant effect on cancer treatment. However, biomedical functions and molecular mechanisms of tigecycline in human pancreatic ductal adenocarcinoma (PDAC) remain unclear. In the current study, we tried to assess the effect of tigecycline in PDAC cells. AsPC-1 and HPAC cells were treated with indicated concentrations of tigecycline for indicated time, and then, MTT, BrdU and soft agar assay were used to test cell proliferation. The effect of tigecycline on cell cycle and cellular apoptosis was tested by cytometry. Migration and invasion were detected by wound healing assay and transwell migration/invasion assay. Expressions of cell cycle-related and migration/invasion-related protein were determined by using Western blot. The results revealed that tigecycline observably suppressed cell proliferation by inducing cell cycle arrest at G0/G1 phase and blocked cell migration/invasion via holding back the epithelial-mesenchymal transition (EMT) process in PDAC. In addition, tigecycline also remarkably blocked tumorigenecity in vivo. Furthermore, the effects of tigecycline alone or combined with gemcitabine in vitro or on PDAC xenografts were also performed. The results showed that tigecycline enhanced the chemosensitivity of PDAC cells to gemcitabine. Interestingly, we found CCNE2 expression was declined distinctly after tigecycline treatment. Then, CCNE2 was overexpressed to rescue tigecycline-induced effect. The results showed that CCNE2 overexpression

Dihydrocapsaicin Inhibits Cell Proliferation and Metastasis in Melanoma via Down-regulating β-Catenin Pathway

“…The xenograft tumors were immobilized, dehydrated, and paraffin embedded, 5-μm thick sections were stained with β-catenin (1:400; Cell Signaling) and Ki67 (1:200; Abcam) for IHC analysis. Detailed steps were performed with reference to a previously study ( 33 ).…”

Insights Into the Molecular Mechanism of Deer Antler Extract Serving as a Potential Chondroprotective Agent for Articular Cartilage

“…Mug1 serves as an inhibitor of proteolytic enzyme that prevents the degradation of cartilage extracellular matrix [56]. In addition, Cdc25b, Mki67, Bub1, Ccne2, Mphosph8, G2e3, Dyrk3 and Cep70 are considered to be essential genes involved in cell proliferation [57][58][59][60][61][62][63]. Thus, these results suggest that DAE play a potential role in regulating articular cartilage formation, growth and repair by controling multiple functional genes involved in chondrocyte commitment, survival, proliferation and differentiation.…”

Investigating the molecular control of deer antler extract on articular cartilage 

“…Mug1 serves as an inhibitor of proteolytic enzyme that prevents the degradation of cartilage extracellular matrix [58]. In addition, Cdc25b, Mki67, Bub1, Ccne2, Mphosph8, G2e3, Dyrk3 and Cep70 are considered to be essential genes involved in cell proliferation [59][60][61][62][63][64][65]. Thus, these results suggest that DAE might serve as a candidate supplement for maintaining cartilage homeostasis.…”