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.
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.
We found that MBD1 expression was significantly upregulated in gallbladder cancer tissues compared with that in surrounding normal tissues according to immunohistochemical analysis of 84 surgically resected gallbladder cancer specimens.
The clinicopathologic analyses showed PLEK2 expression was positively correlated with tumor TNM stage, distant metastasis and PLEK2 was an independent predictor of overall survival (OS) in GBC patients.
<b>Conclusions:</b> We found a highly reliable FI network, which revealed <i>LIFR, PIK3R1</i>, and <i>MMP12</i> as novel prognostic biomarker candidates for GBC.
Following inhibition of the expression of Bmi-1 in gallbladder cancer cell line GBC-SD, the growth cycle of cancer cells was prolonged and apoptotic rate increased.
Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up-regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines.
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.
Finally, the lncRNA-miRNA-gene ceRNA network was constructed by combining the three types of relation pairs, such as XLOC_011309-miR-548c-3p-SPOCK1 and XLOC_012588-miR-765-CEACAM6. mRNAs and lncRNAs may be involved in gallbladder cancer progression via ECM-receptor interaction pathways and the complement and coagulation cascades.
Collectively, these data indicates that miR-181b possibly mediates the pathologic progression of GBC by CREBRF/CREB3 signaling pathways and impairs anti-tumor effects of Rg3 on GBC development, which suggests that miR-181b might be an key switch in the process of Rg3-mediated tumor cytotoxicity in the progression of GBC.
While in IDH1-2/BAP1/PBRM1 group there were 58%, 22%, and 10% of patients with intrahepatic-cholangiocarcinoma (ICC), perihilar-cholangiocarcinoma (PHCC), and gallbladder cancer (GBC), in KRAS/TP53 group there were 42%, 78%, and 90% of patients with ICC, PHCC, and GBC (p = 0.003), respectively.