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Background Gastric cancer (GC) is a common malignant disease worldwide. Aberrant miRNAs expression contributes to malignant cells behaviour, and in preclinical research, miRNA targeting has shown potential for improving GC therapy. Our present study demonstrated that miR-632 promotes GC progression in a trefoil factor 1 (TFF1)-dependent manner. Methods We collected GC tissues and serum samples to detect miR-632 expression using real-time PCR. A dual-luciferase reporter assay was used to identify whether miR-632 directly regulates TFF1 expression. Tube formation and endothelial cell recruitment assays were performed with or without miR-632 treatment. Western blot and in situ hybridization assays were performed to detect angiogenesis and endothelial recruitment markers that are affected by miR-632. Results Our results showed that miR-632 is highly expressed in GC tissue and serum and negatively associated with TFF1 in GC. miR-632 improves tube formation and endothelial cell recruitment by negatively regulating TFF1 in GC cells. Recombinant TFF1 reversed miR-632-mediated angiogenesis. TFF1 is a target gene of miR-632. Conclusions Our study demonstrated that miR-632 promotes GC progression by accelerating angiogenesis in a TFF1-dependent manner. Targeting of miR-632 may be a potential therapeutic approach for GC patients.

In addition to maintaining immune tolerance, Foxp3+ regulatory T cells (Tregs) perform specialized functions in tissue homeostasis and remodeling. However, whether Tregs in aortic aneurysms have a tissue‐specific phenotype and function is unclear. Here, a special group of Tregs that potentially inhibit abdominal aortic aneurysm (AAA) progression are identified and functionally characterized. Aortic Tregs gradually increase during the process of AAA and are mainly recruited from peripheral circulation. Single‐cell TCR sequencing and bulk RNA sequencing demonstrate their unique phenotype and highly expressed trefoil factor 1 (Tff1). Foxp3cre/creTff1flox/flox mice are used to clarify the role of Tff1 in AAA, suggesting that aortic Tregs secrete Tff1 to regulate smooth muscle cell (SMC) survival. In vitro experiments confirm that Tff1 inhibits SMC apoptosis through the extracellular signal‐regulated kinase (ERK) 1/2 pathway. The findings reveal a tissue‐specific phenotype and function of aortic Tregs and may provide a promising and novel approach for the prevention of AAA. A group of Tregs with a tissue‐specific phenotype and function potentially protects abdominal aortic aneurysm progression via Tff1.

Several stomach diseases are attributed to the dysregulation of physiological function of gastric mucosal barrier by pathogens. Gastric organoids are a promising tool to develop treatment strategies for gastric infections. However, their functional features of in vivo gastric mucosal barrier and host–microbe interactions are limited due to the lack of physiological stimuli. Herein, a human stomach micro‐physiological system (hsMPS) with physiologically relevant gastric mucosal defense system is described based on the combination of organoid and MPS technology. A fluid flow enhanced epithelial‐mesenchymal interaction in the hsMPS enables functional maturation of gastric epithelial cells, which allows for the recreation of mesh‐like mucus layer containing high level of mucus protective peptides and well‐developed epithelial junctional complexes. Furthermore, gastroprotection mechanisms against Helicobacter pylori (H. pylori)  are successfully demonstrated in this system. Therefore, hsMPS represents a new in vitro tool for research where gastric mucosal defense mechanism is pivotal for developing therapeutic strategies.

Forkhead box A1 (FOXA1) plays an important role in the central nervous system, and its loss can lead to the downregulation of tyrosine hydroxylase, which directly affects the synthesis of dopamine, thus leading to Parkinson's disease (PD). The present study aimed to explore the specific role of FOXA1 in PD. Blood samples from patients with PD were collected to determine the expression levels of FOXA1 using reverse transcription-quantitative PCR (RT-qPCR). In addition, mouse dopaminergic neuron MES23.5 cells were induced with 6-hydroxydopamine (6-OHDA) to construct an in vitro PD model in order to study the effect of FOXA1 overexpression on cell inflammation, oxidative stress and apoptosis with RT-qPCR, assay kits and TUNEL assays, respectively. Subsequently, the expression of FOXA1 was silenced to assess the effect on the downstream mechanism. The results revealed that the expression level of FOXA1 was downregulated in patients with PD, and FOXA1 overexpression attenuated 6-OHDA-induced inflammation, oxidative stress and apoptosis in MES23.5 cells. Furthermore, FOXA1 could bind to the trefoil factor 1 (TFF1) promoter, and the effects of FOXA1 overexpression on cells were reversed by TFF1 silencing, indicating that TFF1 mediated the mechanism of FOXA1 overexpression in MES23.5 cells. In conclusion, following FOXA1 transcription, TFF1 expression was activated, thereby relieving 6-OHDA-induced cell inflammation, oxidative stress and apoptosis. The present findings suggested that FOXA1 may serve as a target for the treatment of PD.

Helicobacter pylori (H. pylori) infection has been associated with non-cardia adenocarcinoma in the stomach, while its role in gastric cardia adenocarcinoma (GCA) remains controversial. In addition, the association between H. pylori and the protective factors trefoil factor 1 (TFF1) and gastrokine 2 (GKN2) in gastroesophageal adenocarcinomas has not been fully investigated. Therefore, the mRNA and protein expression levels of TFF1 and GKN2 in GCA and distal gastric adenocarcinoma (DGA) were analyzed using quantitative PCR (qPCR) and immunohistochemistry, and the association with H. pylori infection was investigated. In addition, the effects of TFF1 and GKN2 overexpression on H. pylori-induced cells were investigated using western blot and reverse transcription-qPCR analysis. The comparative analysis of 16S rRNA-positive mRNA expression between GCA and DGA showed no statistically significant difference. However, the rate of the H. pylori vacuolating toxin A (VacA) genotype was significantly higher in GCA (49.2%) compared with that in DGA (26.9%; P<0.05). H. pylori infection downregulated the mRNA and protein expression levels of TFF1 and GKN2 in gastric tumor tissues, and the mRNA expression level of TFF1 and GKN2 was also markedly decreased in vitro. Furthermore, the cell proliferation varied in H. pylori total protein treatment group with the different doses. Notably, treatment with 20 µg/ml H. pylori total protein for 24 h resulted in the highest cellular proliferation rate. In addition, TFF1 and GKN2 overexpression inversely inhibited H. pylori-induced cell proliferation and upregulated NF-κB, tumor necrosis factor-α, IL-1β, IL-2, IL-4 and IL-6. The results of the present study indicate that H. pylori, particularly the VacA+ strain, plays an important role in GCA pathogenesis in high-risk areas of China, while TFF1/GKN2 inhibits H. pylori-induced cell proliferation and inflammation in GCA and DGA.

Antibodies are important tools in anatomical pathology and research, but the quality of in situ protein detection by immunohistochemistry greatly depends on the choice of antibodies and the abundance of the targeted proteins. Many antibodies used in scientific research do not meet requirements for specificity and sensitivity. Accordingly, methods that improve antibody performance and produce quantitative data can greatly advance both scientific investigations and clinical diagnostics based on protein expression and in situ localization. We demonstrate here protocols for antibody labeling that allow specific protein detection in tissues via bright-field in situ proximity ligation assays, where each protein molecule must be recognized by two antibodies. We further demonstrate that single polyclonal antibodies or purified serum preparations can be used for these dual recognition assays. The requirement for protein recognition by pairs of antibody conjugates can significantly improve specificity of protein detection over single-binder assays.

Purpose This study aims to evaluate the potential of Trefoil Family Factor 1 (TFF1) as a biomarker for the diagnosis and prognosis of retinoblastoma. Methods Our protocol was prospectively registered on PROSPERO (CRD420251126954). On July 08, 2025, we conducted a comprehensive literature search across PubMed, Scopus, Web of Science, Embase, Cochrane, and Google Scholar. We included all studies that measured TFF1 expression in retinoblastoma patients and assessed its potential as a biomarker for disease severity. The primary outcomes were laterality, sex, and age at diagnosis. Secondary outcomes included tumor invasion and disease staging. Statistical analysis was performed using RStudio. A random-effects model was used for the analysis, and heterogeneity was assessed using the I². The risk of bias for the included studies was evaluated using the Newcastle-Ottawa Scale for Retrospective cohort studies, while the NIH Quality Assessment Tool for Case Series Studies was used for case series studies. Results Of the 152 articles initially identified, only 5 met the inclusion criteria, comprising a total of 521 patients with retinoblastoma. Patients with higher TFF1 expression exhibited a significantly lower risk of bilateral involvement (RR = 0.57; 95% CI: 0.39, 0.84; p  = 0.0041) and a significantly higher association with being diagnosed after the age of 3 years (RR = 4.26; 95% CI: 1.33, 13.64; p  = 0.01). No statistically significant associations were observed with sex (RR = 0.89; 95% CI: 0.74,1.07; p  = 0.2), choroid invasion (RR = 0.99; 95% CI: 0.9,1.08; p  = 0.76) or optic nerve invasion including no invasion (RR = 0.75; 95% CI: 0.47,1.21; p  = 0.24), pre-laminar invasion (RR = 1.13; 95% CI: 0.75,1.7; p  = 0.55) or post laminar invasion (RR = 1.04; 95% CI: 0.89,1.21; p  = 0.61). Conclusion Retinoblastoma tumors with higher TFF1 expression were associated with a reduced risk of bilateral involvement and an increased likelihood of diagnosis after the age of 3 years. Although the associations with choroidal and optic nerve invasion were not statistically significant, TFF1 remains a promising candidate biomarker for the diagnosis and prognosis of retinoblastoma, particularly due to its absence in normal ocular tissue. Further high-quality studies are required to validate the clinical utility of TFF1 as a reliable diagnostic and prognostic marker in retinoblastoma.

Objectives The distinction between metastatic breast carcinomas (BCs) and primary lung carcinomas (PLCs) can be difficult. This study tested the utility of trefoil factor 1 (TFF1) for this purpose and compared it with mammaglobin and GATA protein binding 3 (GATA-3). Methods Tissue microarrays containing 365 BCs and 338 PLCs were stained with TFF1, mammaglobin, and GATA-3, and an H-score was calculated. Sensitivity, specificity, and accuracy were calculated, and logistical regression analysis was performed. Results Accuracy of correctly classifying the tumor type was 81.9%, 71.3%, and 64.0% for GATA-3, mammaglobin, and TFF1, respectively. Odds ratios for selecting BCs were 25.69, 93.15, and 4.17, respectively, with P values less than .001. With a single exception, the best immunopanel included GATA-3 and mammaglobin in all comparisons. Conclusions TFF1 demonstrated breast specificity but was inferior to mammaglobin and GATA-3. Therefore, its routine clinical use may not be justified. TFF1 showed little benefit when added to an immunopanel.

TFF1 expression is markedly reduced in human GCs, suggesting that TFF1 is a tumor suppressor for human gastric cancer. The present study evaluated the expression and distribution pattern of TFF1 in paraffin-embedded canine gastric tissue samples, including normal mucosa (n = 3), polyps (n = 8), carcinomas (n = 31) and their adjacent non-neoplastic mucosa (n = 30), neoplastic emboli (n = 14), and metastatic lesions (n = 9), by immunohistochemistry (IHC). All normal gastric tissues expressed TFF1 in the superficial foveolar epithelium and mucopeptic cells of the neck region. Most gastric polyps (GPs) displayed immunoreactivity for TFF1 in >75% of the epithelial component. In GCs, the expression of TFF1 was found reduced in 74.2% of the cases. The level of TFF1 expression had a decreased tendency from normal gastric mucosa to GPs and GCs (p < 0.05). No significant differences in the expression of TFF1 were found in GCs, according to age, sex, histological type based on World Health Organization (WHO) and Lauren classification, tumor location, depth of tumor invasion, presence of neoplastic emboli or metastatic lesions. The median survival time of GC patients with preserved and reduced TFF1 immunoexpression were 30 and 12 days, respectively. Kaplan–Meier analysis revealed no significant survival differences between the two groups (p > 0.05). These findings suggest that TFF1 protein may play a role in canine gastric carcinogenesis, and further studies are necessary to define its usefulness as a prognostic indicator in canine gastric carcinoma.

Trefoil factor 1 (TFF1) is a small secretory protein expressed in various types of carcinomas including breast cancer. The TFF1 gene contains an estrogen response element and its expression can be regulated by estrogen. Previous reports showed that TFF1 could protect cells from induced apoptosis in vitro. In the present study, the effect of estrogen on the promotion of doxorubicin-induced apoptosis resistance and the role of TFF1 in this process was demonstrated using the MCF-7 breast cancer cell model. Stable knockdown of the TFF1 gene in MCF-7 cells was generated and used to test the sensitivity to doxorubicin treatment compared to mock control cells in the presence or absence of 17β-estradiol. The apoptotic cells were measured by flow cytometry. The results showed that with the stimulation of apoptosis by doxorubicin, 17β-estradiol could suppress this process in mock cells but not in TFF1 knockdown cells. Moreover, using a viable cell counting method, it was shown that the anti-TFF1 antibody could reverse the anti-apoptotic effect of estrogen in mock cells and recombinant TFF1 could recover doxorubicin-induced cell death in TFF1 knockdown cells. This process, however, could not be inhibited by fulvestrant, an estrogen antagonist. An apoptosis protein array experiment reflected the role of the anti-oxidative enzyme catalase in estrogen and TFF1-modulated apoptosis and this was confirmed by enzymatic assay. These phenomena determine the role of TFF1 in estrogen-promoted resistance to apoptosis induced by doxorubicin in MCF-7 breast cancer cells. The TFF1 gene may be a target for enhancing the sensitivity to chemotherapy in breast cancer treatment.