The effect of CYP1A1 IVS1 + 606 on gallbladder cancer was more pronounced among non-obese (body mass index < 23) (OR = 3.3, 95% CI = 1.8-6.1; P interaction = 0.001).
Specifically, variants in the IL8, IL8RB, RNASEL, and NOS2 genes were associated with biliary stones, whereas VEGF variants were associated with gallbladder cancer.
These results suggest that the Val allele of CYP1A1Ile462Val polymorphism and the Pro allele of TP53 Arg72Pro polymorphism contribute to an increased risk of GBC among Japanese women and men, respectively.
Preoperative serum IL-6 is significantly associated with prognostic implications in patients with hepatic side T2 GBC, not in those with peritoneal side tumors.
Of these, 147/175 (18 lung, 43 oral, 13 esophageal and 73 gallbladder) cancer patients (84%) showed higher IL-6 levels as compared to control group (normal range: <7 pg/ml).
IL-6 and IL-10 were significantly increased in both the HCC and GBC groups, IL-2, IL-6, IL-10, and TNF-<i>α</i> in the cholangiocellular carcinoma group, and IL-2, IL-6, IL-8, and TNF-<i>α</i> in the pancreatic cancer group.
We identify that inflammatory cytokine, IL-6 promotes proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of GBC both in vitro and in vivo.
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).
These results suggest that TNFA -308 (G/A) polymorphism may influence the susceptibility of female gender gallbladder cancer in absence of gallstones while IL6-174 G/C polymorphism does not seem to be playing significant role in the susceptibility to gallbladder cancer.
Consistent with this, treatment with ERBB2-specific, EGFR-specific shRNA or with a covalent EGFR family inhibitor Afatinib inhibits tumor-associated characteristics of the gallbladder cancer cells.
Real‑time quantitative polymerase chain reaction analysis and immunohistochemistry experiments revealed that HIF‑1α was significantly upregulated in GBC tissues.
In conclusion, miR-143-3p suppresses tumour angiogenesis and growth of GBC through the ITGA6/PI3K/AKT/PLGF pathways and may be a novel molecular therapeutic target for GBC.
In conclusion, miR-143-3p suppresses tumour angiogenesis and growth of GBC through the ITGA6/PI3K/AKT/PLGF pathways and may be a novel molecular therapeutic target for GBC.
In conclusion, miR-143-3p suppresses tumour angiogenesis and growth of GBC through the ITGA6/PI3K/AKT/PLGF pathways and may be a novel molecular therapeutic target for GBC.
In conclusion, miR-143-3p suppresses tumour angiogenesis and growth of GBC through the ITGA6/PI3K/AKT/PLGF pathways and may be a novel molecular therapeutic target for GBC.