UCP2 knockdown suppressed the activation of the NF-κB/β-catenin axis and promoted the increases in mitochondrial ROS in gallbladder cancer cells exposed to gemcitabine treatments.
Our findings indicate that miR-7-2-3p and miR-29c-3p play crucial roles in the pathogenesis and worse prognosis of GBCs, which may serve as prognosis biomarkers and promise potential therapeutic targets in the future.
SSTR5-AS1 is significantly increased in GBC samples and cell lines, especially in gemcitabine-resistant cell lines, and higher SSTR5-AS1 expression was correlated with poorer overall survival rate in GBC patients.
The serum γ-GGT levels were higher in IgG4-C patients than in GBC patients, whereas the serum levels of CA125 were significantly higher in GBC patients than in IgG4-C patients.
The gallbladder cancer SGC996 cell line was transfected with claudin-1-RNA interference lentivirus (LV-CLDN1-RNAi) to downregulate claudin-1 expression, and the downstream effects on cell proliferation, the cell cycle, apoptosis and cell invasion were investigated.
Immunohistochemistry (IHC) staining analysis and quantitative real-time PCR (qRT-PCR) were conducted to determine the expression of SLC25A22 in GBC tissues.
The serum γ-GGT levels were higher in IgG4-C patients than in GBC patients, whereas the serum levels of CA125 were significantly higher in GBC patients than in IgG4-C patients.
The present study systematically examined the genes implicated in cholesterol homeostasis, and revealed altered gene expressions of <i>de novo</i> cholesterol biosynthesis and sterol sulfonation (SULT2B1), reduced bile acid synthesis (CYP7B1 and CYP39A1) and impaired sterol efflux (ABCA1, ABCG5, LCAT, and CETP) in GBC tissues.
Here we found that KPNA2 was significantly upregulated in gallbladder cancer (GBC), and the increased levels were correlated with short survival of patients.
The efficacy of apatinib, an highly potent and selective oral inhibitor of VEGFR-2 tyrosine kinase, for refractory advanced GBC has not yet been clarified.