Celecoxib treatment led to G1 arrest via the upregulation of p21 and p27 expression in GBC-SD and NOZ cells, whereas PD184161 did not affect cell cycle distribution.
A very high frequency of GBC methylation was detected in SEMA3B (46/50, 92%) and FHIT (33/50, 66%), intermediate incidences in BLU (13/50, 26%) and DUTT1 (11/50, 22%) and very low frequencies in RASSF1A (4/50, 8%) and hMLH1 (2/50, 4%).
In conclusion, our studies suggest that baicalein may be a potential phytochemical flavonoid for therapeutics of GBC and ZFX may serve as a molecular marker or predictive target for GBC.
Mechanical investigations verified PLZF could regulate the expression of cell cycle arrest-associated gene p21 and epithelial-mesenchymal transition (EMT)-related genes (E-cadherin and N-cadherin) in GBC cell lines.
This study was aimed to examine the role of OGG1 rs1052133" genes_norm="4968">Ser326Cys (rs1052133) and XRCC1rs1799782;s746702110" genes_norm="4968;7515">Arg194Trp (C > T) (rs25487) and rs25487" genes_norm="7515">Arg399Gln (G > A) (rs1799782) polymorphisms in GBC susceptibility.
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.
c‑Jun suppresses the expression of WNT inhibitory factor 1 through transcriptional regulation and interaction with DNA methyltransferase 1 in gallbladder cancer.
In contrast, the GBd15 and FU-GBC-1 cell lines treated with EGF and HGF showed a scattering phenotype, and expressed low levels of ECD and high levels of SNAIL, vimentin, TGF-β, and NS.
Higher mRNA expression levels of IL‑6, Twist and Vimentin and a reduced expression level of E‑cadherin were also demonstrated in the GBC tissues (P<0.05).
Taken together, TNF-α can upregulate the expression of VEGF-C and promote the lymphangiogenesis of GBC via NF-κB combining with the promoter of VEGF-C.
The results revealed a significantly increased sVEGF-C level in patients with GBC compared with the healthy donors, however no statistically significant difference was identified between patients with GBC and chronic cholecystitis. sVEGF-C levels were associated with lymph node metastasis in GBC and presented a positive correlation with VEGF-C expression and lymphatic vessel density (LVD) in patients with GBC.
Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer.