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.
<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.
In addition, we found that the STAT1-regulated protein IRF7 is downregulated in GBC compared to normal gallbladder tissue and low IRF7 expression is associated with significantly lower overall survival of GBC patients.
In addition, we found that the STAT1-regulated protein IRF7 is downregulated in GBC compared to normal gallbladder tissue and low IRF7 expression is associated with significantly lower overall survival of GBC patients.
CircERBB2 regulates nucleolar localization of PA2G4, thereby forming a circERBB2-PA2G4-TIFIA regulatory axis to modulate ribosomal DNA transcription and GBC proliferation.
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.
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.
PLAC8 blockade using siRNA reversed chemotherapy resistance and downregulated MRP and MDR1 in SGC966GR and SGC966OR cells, suggesting that PLAC8 mediates chemotherapy resistance in GBC.
The results revealed that NOX1 expression was significantly upregulated in the stroma of GBCs compared with precancerous and benign lesions of the gallbladder; NOX1 expression was localized to gallbladder stromal fibroblasts expressing α‑smooth muscle actin and fibroblast secreted protein‑1.
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 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.
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.
<b>Methods:</b> Activities of CTSL and CTSB were assayed in the gallbladder (GB) tissues obtained from GBC patients (<i>n</i> = 43) and control subjects (<i>n</i> = 69).
<b>Methods:</b> Activities of CTSL and CTSB were assayed in the gallbladder (GB) tissues obtained from GBC patients (<i>n</i> = 43) and control subjects (<i>n</i> = 69).
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.