TFF1 antibody
- Known as:
- TFF1 (anti-)
- Catalog number:
- orb100742
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- TFF1 antibody
Related genes to: TFF1 antibody
- 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 antibody
Related articles to: TFF1 antibody
- Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer characterized by limited treatment options and poor prognosis. While TNBC exhibits a lower incidence of bone metastasis compared to luminal subtypes, its occurrence is associated with substantial morbidity and mortality. The metabolic mechanisms enabling TNBC cells to colonize bone remain largely undefined. In this study, a bone-tropic TNBC subline (MDA-MB-231/BM) was developed through iterative intracardiac inoculation in mice, followed by transcriptomic profiling to identify genes with altered expression. A CRISPR/Cas9 knockout library screen in MDA-MB-231 cells further revealed critical regulators of bone metastasis. Notably, dual-omics analysis demonstrated a consistent downregulation of key enzymes in the tricarboxylic acid (TCA) cycle within bone-metastatic TNBC cells. Functional experiments showed that PDHA1 knockout impaired cell migration, invasion, and mitochondrial respiration, underscoring the TCA cycle's essential role in metastasis. Among the identified regulators, TFF1 emerged as a potent suppressor of TCA cycle gene expression. Deletion of TFF1 enhanced mitochondrial function, reduced metastatic burden in vivo, and extended survival in mouse models. Supporting clinical relevance, TCGA data showed significantly higher TFF1 expression in luminal breast cancer compared to TNBC, aligning with the greater propensity for bone metastasis in luminal subtypes. These findings reveal that TFF1-mediated suppression of the TCA cycle contributes to the metabolic adaptation of TNBC cells for bone colonization, offering a potential therapeutic vulnerability and advocating for subtype-specific metabolic interventions. - Source: PubMed
Publication date: 2026/06/09
Chen HanshenXu YipingLiu YixuanTang YijieQiu JiapengLei LuyaoLin PeichengChen YiranWu Xiaodan - Estrogen receptor alpha (ERα) plays a crucial role in the proliferation and survival of ER-positive breast cancer cells, and tamoxifen (TAM) remains the mainstay of endocrine therapy. However, acquired resistance to TAM remains a major clinical challenge. Despite advances in molecular profiling and targeted therapies, the mechanisms underlying TAM resistance remain incompletely understood. Emerging evidence suggest that dysregulation of intracellular signaling pathways, including the cAMP/CREB axis, may contribute to endocrine therapy failure. - Source: PubMed
Publication date: 2026/05/28
Kim Bu GyeomKim OkhyeonLee Do-YeonKim Bo RamKim Dae YeongNamgung YoonBong Jun WooKang SangheeLee Sun IlOh Sang Cheul - : Gastric signet-ring cell carcinoma (GSRCC) is an aggressive gastric cancer subtype with abundant mucin production and high metastatic propensity. However, scarcity of specific biomarkers has impeded clinical diagnosis and mechanistic research. This study systematically compares GSRCC and gastric adenocarcinoma (AC) to identify biomarkers and elucidate molecular basis of GSRCC's aggressive behavior. : We performed single-cell RNA sequencing (scRNA-seq) on surgically resected primary GC tissues, validating our findings using public datasets and functional experiments. : We identified expansion of a mucin-secreting epithelial subcluster (Mucous_muc5ac) in GSRCC, characterized by high , , and other prognosis-associated genes. Within this population, a MUCL3 subpopulation (Cluster 1) spatially corresponded with classic signet-ring morphology, validating MUCL3 as a specific marker for these cells. Multi-omics analysis revealed that MUCL3 signet-ring cells exhibit genomic instability, dedifferentiation, and enrichment of TNF-α/NF-κB, TGF-β/EMT, and hypoxia pathways, with elevated metastasis/angiogenesis gene scores and high expression. Functional validation confirmed that TFF1 was associated with increased gastric cancer cell migration. : Our study characterizes the MUCL3 signet-ring cell subpopulation, highlighting the diagnostic utility of MUCL3 and suggesting TFF1 as a candidate for further investigation. These findings establish a foundation for advancing precision diagnosis and mechanistic understanding of GSRCC. - Source: PubMed
Publication date: 2026/05/08
Zhang JieWang YinpingYuan TingWu WenguangLi XuechuanHou ZhaoyuanLi MaolanLiu Yingbin - Transcriptional bursts regulate gene expression by altering burst size or burst frequency. Here, we present a protocol that integrates fixed-cell smFISH and live-cell single-molecule imaging to analyze estrogen-responsive transcriptional bursting of the TFF1 gene in human breast cancer cell lines. This workflow enables measurement of burst size, burst initiation, and active allele frequency to determine how endocrine disruptor chemicals modulate transcriptional bursting dynamics. For complete details on the use and execution of this protocol, please refer to Day, Yasar et al.. - Source: PubMed
Publication date: 2026/05/05
Yasar PelinDay Christopher RRodriguez Joseph - Excessive activation of the estrogen receptor (ER) drives proliferation, progression, and the formation of breast cancer stem cells (CSCs) in ER-positive breast cancer. Estrogenic endocrine disrupting compounds (EDCs) found in plastics, water, and food are also able to bind to the ER. Thus, we hypothesized that estrogenic EDCs mimic estrogen (E2) in the pathogenesis of breast cancer by promoting their survival and proliferation. Three estrogenic EDCs routinely found in human biosamples were selected for analysis: bisphenol-A (BPA), diethyl-hexyl phthalate (DEHP), and alpha-zeranol (αZAL). We assessed proliferation, transcriptional reprogramming, and CSC formation in breast cancer cell lines. E2, BPA, and αZAL significantly increased cell proliferation in ER-positive, but not ER-negative cell lines. This was reversed after administration of the ER-antagonist, ICI 182,780. BPA and αZAL upregulated estrogen target genes (PGR, TFF1) and increased levels of cell-cycle protein. RNA sequencing analysis revealed that BPA and αZAL altered expression of genes related to cell division, DNA repair, and estrogen signaling, with a substantial transcriptional overlap between EDCs and estrogen treatments. Additionally, BPA and αZAL increased the proportion of CSCs, defined as the CD24/CD44 expressing subpopulation. Overall, these data indicate that BPA and αZAL act as functional estrogen mimics in breast cancer cells, activating canonical estrogen signaling pathways and promoting stem-like characteristics. Notably, this study provides the first transcriptomic and stem-associated characterization of αZAL in ER-positive breast cancer cells, revealing a robust estrogenic mode of action. This work provides mechanistic insight into how environmental EDCs may influence ER-positive breast cancer biology. - Source: PubMed
Publication date: 2026/05/03
Winz CassandraLi EricXie CarolineLee Kyo ChangBoguszewski KevinRohatagi ShlokHahn RitaRancourt RayFurmanski PhilipSuh Nanjoo