Ask about this productRelated genes to: TFF1 Blocking Peptide
- Gene:
- TFF1 NIH gene
- Name:
- trefoil factor 1
- Previous symbol:
- BCEI
- Synonyms:
- D21S21, HPS2, pS2, pNR-2, HP1.A
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: TFF1 Blocking Peptide
Related articles to: TFF1 Blocking Peptide
- Aberrant alternative splicing (AS) in cancer generates oncogenic proteomic diversity that drives tumor progression. Given the suboptimal efficacy of immune checkpoint inhibitors (ICIs) in gastric cancer (GC), the therapeutic potential of modulating RNA splicing to augment immunotherapy remains unclear. Here, we demonstrate that the splicing factor SRSF10 is progressively upregulated during gastric tumorigenesis and exhibits elevated expression in ICIs-resistant GC. Utilizing multiple mouse models, we confirmed that SRSF10 ablation with a selective inhibitor 1C8 robustly inhibits GC growth and enhances CD8 T-cell infiltration via CCL2-mediated reprogramming of tumor-associated macrophages (TAMs). Notably, SRSF10 blockade restricts pre-neoplastic metaplastic cells re-entry the cell cycle and the TAMs reprogramming. Mechanistically, cell-autonomous SRSF10 activates mTOR signaling primarily through inclusion of exon 2 in the BCAA transaminase 2 (BCAT2) mRNA. Pharmacological antagonism of SRSF10 potentiated the therapeutic effect of anti-PD-1 antibody in Tff1-CreER; Apc; p53 orthotopic GC models. Collectively, our findings revealed that SRSF10 orchestrates mTOR-CCL2 signaling by alternative RNA splicing of BCAT2 to reprogram TAMs, proposing SRSF10 as a tempting therapeutic target for GC immunotherapy. - Source: PubMed
Publication date: 2026/04/22
Huang Xiao-BoYang Xin-PengZheng Hua-LongWang Ling-QianJiang Chen-YangChen Yun-LinLin BinLi Yi-FanGuo Xiao-JingHuang QiangGao You-XinLi YiYe Xiao-QianWang Jia-BinXie Jian-WeiLin Jian-XianZheng Chao-HuiHuang Chang-MingChen Qi-YueLi Ping - TFF1 is a secretory polypeptide that is typical of mucous epithelia belonging to the trefoil factor family (TFF) of lectins. Originally, was discovered as an estrogen-responsive gene in breast cancer cell lines. However, its major physiological expression site is the stomach where it exists mainly in a monomeric form, with minor amounts of homodimeric as well as heterodimeric forms, such as a high-molecular-mass complex with IgG Fc binding protein (FCGBP). For the first time, we characterized different low-molecular-mass forms of TFF1 in human post-menopausal vaginal specimens, i.e., monomeric and dimeric forms. Attempts to identify high-molecular-mass forms of TFF1, such as TFF1-FCGBP, failed. Based on its known anti-inflammatory effects, TFF1 could play an important role in the homeostasis of vaginal microbiota, which is normally predominated by spp. Due to its lectin activity, TFF1 might also be capable of binding to members of the vaginal microbiota or to vaginal fungal pathogens. This points to a potential role for TFF1 in the vagina's innate immune defence and could be of clinical relevance particularly after menopause, e.g., for the treatment of bacterial vaginosis or vulvovaginal candidiasis, as here vaginal dysbiosis is often observed as a consequence of estrogen deficiency. - Source: PubMed
Publication date: 2026/03/18
Laskou AikateriniHarder SönkeZnalesniak Eva BSchlüter HartmutKünnemann InesTchaikovski Svetlana NHoffmann Werner - This study aims to evaluate the potential of Trefoil Family Factor 1 (TFF1) as a biomarker for the diagnosis and prognosis of retinoblastoma. - Source: PubMed
Publication date: 2026/03/26
Alqedra JawadElarnaut LinaEthman Abdulrahman BinElnahry Ayman GSerhan Hashem AbuElhadi Muhammed - infection is the main risk factor for gastric cancer. easily develop antibiotic resistance and evade host defenses. In-depth knowledge of the first barrier that encounter, the gastric surface mucus-producing epithelial cells (SMCs), may enable improved treatment and prevention. This study aimed to characterize SMC gene expression, mucus glycosylation, and identify how colonization affects these parameters. The glycosylation of eight -infected and eight sham control mice was characterized by mass spectrometry. SMCs from five infected and five sham control mice were extracted with laser microdissection (LCM) and sequenced with RNA sequencing (RNA-Seq). SMCs were characterized by high gene expression for proteins secreted into mucus (, , , , and , mitoribosome RNA, and cytoskeleton proteins. Mucin glycans were large, complex, heavily fucosylated, and dense with H-antigen motifs. Two main glycosylation pathways ending in H-antigen glycans were identified and corroborated with glycosyltransferase expression. Glycosylation was consistent between -infected and sham control mice. RNA-Seq data was analysed for differential gene expression, gene set enrichment analysis, and network analysis of functionally-related genes. The analyses revealed that genes required for protein synthesis and oxidative phosphorylation were down-regulated in infected mice. Most up-regulated genes were either interferon-stimulated genes or able to induce interferon production themselves. Depletion of Nkx6-3 occurred in the infected mice, indicating initiation of a pre-cancerous cascade. LCM RNA-Seq of SMCs was thus feasible and enabled characterization of the SMC and definition of a gene set showing how infection affects SMCs. - Source: PubMed
Publication date: 2026/03/25
Erhardsson MattiasSantos LicíniaBenktander JohnSharba SinanThorell KaisaLindén Sara - Proteomic changes can provide critical insights into the molecular alterations underlying epilepsy. Recent advances in proteomic technologies present opportunities to identify novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/02/26
Yao YuanZou QinChen Ke