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Study findings demonstrate a functional role of TFF1 in suppressing gastric tumorigenesis by impeding the IL6-STAT3 pro-inflammatory signaling axis.
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This study indicates that the acquisition of TFF1 expression is an early event in pancreatic carcinogenesis and that TFF1 might act as a tumor suppressor to prevent EMT and the invasive transformation of PanIN.
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Study indicates that loss of TFF1 promotes the aberrant overexpression of HOXA10 and miR-196b by demethylation of the HOXA10 promoter, which provides a new perspective of TFF1/HOXA10/miR-196b functions in human gastric cancer.
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TFF1 is responsible for liver regeneration after liver injury by promoting the differentiation of hepatic progenitor cells (HPC) into a biliary lineage and inhibiting HPC differentiation into a hepatic lineage.
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our findings demonstrate overexpression of TIMP1 in mouse and human gastric cancers through NF-kB-dependent mechanism. We also show that TFF1 suppresses NF-kappaB and inhibits TIMP1-mediated proliferative potential in gastric cancer.
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H. pylori upregulates GATA-5 mRNA levels after 6, 24, and 48 h of infection in gastric epithelial cells compared to uninfected cells, in parallel with a progressive increase in TFF1 mRNA levels.
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Our study demonstrated that miR-632 promotes Gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner. Targeting of miR-632 may be a potential therapeutic approach for Gastric cancer patients.
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Serum concentrations of TFF1 and TFF3 but not TFF2 are higher in women with breast cancer than in women without breast cancer.
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results suggest that TFF1 and TFF3, but not TFF2, may have a role in breast tumor pathogenesis
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Authors found that rs3761376 AA in the promoter region of TFF1, could reduce the expression of TFF1 by affecting the binding affinity of estrogen receptor 1 (ESR1, ERalpha), and thereby increased the risk of GC (1.29, 1.08-1.53).
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Findings suggest that the hypoxic conditions, which can be induced by gastric injury, promote TFF1 up-regulation, strengthened by an auto-induction mechanism, and that the trefoil peptide takes part in the epithelial-mesenchymal transition events eventually triggered to repair the damage.
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The urine TFF1 and TFF3 levels significantly increased with the progression of chronic kidney disease stages, but not the urine TFF2 levels.
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Study shows that TFF1 expression is silenced in early phases of esophageal squamous cell carcinoma (ESCC) development, which seems to be mediated at least in part by promoter hypermethylation, and provides the basis for the use of TFF1 expression as a potential biomarker for early ESCC detection.
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these data suggest that TFF1 might help cells to counteract Helicobacter colonization and the development of a chronic inflammation.
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Co-expression of GKN2 and TFF1 massively suppressed the expression of positive cell cycle regulators and induced G1/S arrest, synergistically enhancing the inhibition of cell viability and proliferation of gastric cancer cells
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The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 are mechanistically connected to CEBPB and that cross-regulation between CEBPB-RUNX1t1-TFF1 plays an important role in gastric carcinogenesis.
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Low TFF1 expression is associated with retinoblastoma.
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The results suggest that the analysis of expression of MUC5AC and TFF1 may be useful for differentiating sessile serrated adenomas/polyps (SSA/Ps) from hyperplastic polyps (HPs).
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TFF1 displays a distinct protein expression pattern in the developing of airway remodeling due to Sulfur mustard inhalation and plays an important role in maintaining the airway epithelium function
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we found TFF1 plays an oncogenic role in mucinous ovarian cancer