TFF1 Reverse PCR Primer (160bp position)
- Known as:
- TFF1 Reverse PCR test kit Primer (160bp position)
- Catalog number:
- MP1174
- Product Quantity:
- ea
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- TFF1 Reverse PCR Primer (160bp position)
Related genes to: TFF1 Reverse PCR Primer (160bp position)
- 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 Reverse PCR Primer (160bp position)
Related articles to: TFF1 Reverse PCR Primer (160bp position)
- This research sought to investigate the therapeutic efficacy and underlying mechanisms of Shengjiang Powder (SJP) in the context of chronic gastritis. - Source: PubMed
Publication date: 2026/08/14
Liu YihuangLi XiaofengZhang XiaCao HuaZhang NailinSun JianhuiChen Pingping - Colorectal cancer (CRC) remains a leading cause of cancer mortality globally, with therapeutic efficacy hindered by tumor heterogeneity and drug resistance. While organoid technology offers unprecedented opportunities to model tumor complexity, systematic platforms for chemo-targeted combination screening and molecular mechanisms underlying chemoresistance remain underexplored in Chinese populations. Here, we established a biobank of 17 patient-derived CRC organoids (85% success rate) from treatment-naïve surgical specimens, preserving histopathological fidelity and molecular diversity of parental tumors. High-throughput drug screening across eight clinical regimens revealed different responses. To dissect chemoresistance mechanisms, six organoids representing extreme phenotypes (three sensitive and three resistant, based on IC50 difference for irinotecan + raltitrexed) were selected from this cohort for single-cell transcriptomic analysis. Single-cell transcriptomics of irinotecan + raltitrexed-treated organoids identified chemoresistance-associated clonal expansion of epithelial subpopulations (cluster_0), characterized by overexpression of REG4/TFF1/TFF3 and epithelial keratins (KRT19/KRT8/KRT18). Intercellular network analysis revealed intra-epithelial communication as a resistance hub, mediated by 32 ligand-receptor pairs. Integration with TCGA-COAD cohort (n = 378) demonstrated intratumoral heterogeneity (ITH) score as an independent prognostic determinant, outperforming stemness/angiogenesis metrics. Machine learning consensus identified CEACAM6 and KRT19 as dual regulators of mortality and ITH through epithelial plasticity networks. Our multi-omics framework establishes organoid-guided chemoresistance mechanisms while proposing ITH quantification targeting as precision strategies. This study bridges critical gaps in CRC therapeutic personalization, offering clinically actionable insights for overcoming treatment failure. - Source: PubMed
Jing ChangwenWang ZhuoCao HaixiaZhang YuanHuang YuchunYu YuetongLi BingzheMa Rong - Serum trefoil factor 3 (TFF3) has emerged as a promising biomarker for gastric cancer; however, its biological origin remains unclear. - Source: PubMed
Publication date: 2026/07/20
Kuge KomeiMukohyama JunkoYasukawa YoshimiIshibashi YukoMasuda HirokiYasuda TomohikoOhmoto YasukazuTakeshima HideyukiMatsuda AkihisaYoshida HiroshiSeto YasuyukiGoldenring James RUshijima ToshikazuNomura Sachiyo - Aurora kinase A (AURKA) is frequently overexpressed in gastrointestinal cancers. Helicobacter pylori (H. pylori) infection is a significant risk factor for gastric carcinogenesis. LGR5, a stem cell marker in the stomach, plays an important role in gastric tumorigenesis. This study investigates the link between AURKA and LGR5 in response to H. pylori infection in gastric cancer. We analyzed publicly available datasets, gastric cancer cell lines, patient-derived organoids and xenografts (PDOs and PDXs), mouse models, and de-identified human tissue samples. We found a strong association between AURKA and LGR5 expression levels in gastric cancer tissues. In vitro and in vivo analyses showed increased AURKA and LGR5 protein levels in response to H. pylori infection. Using cell models and PDOs, we demontrated an AURKA-dependent induction of LGR5, whereas genetic knockdown or pharmacologic inhibition of AURKA abolished the H. pylori-induced increase in LGR5 by enhancing LGR5 ubiquitination. Mechanistically, AURKA interacted with STAMBP, suppressing LGR5 deubiquitination and thereby promoting its stabilization. Using a tamoxifen-induced conditional knockout (CKO) mouse model of Aurka (Krt19/Aurka), we detected a lower baseline expression of LGR5 in gastric glands, with reduced induction following H. pylori infection, compared to controls. The Aurka CKO mouse model was crossed with the Tff1 model of gastric tumorigenesis to create the Krt19/Aurka /Tff1 mouse model. AURKA knockout, after tamoxifen treatment, significantly reduced the LGR5 protein level and led to a marked decrease in antral thickness. In PDX models, the use of a combination treatment of AMG900 (a pan-AURORA inhibitor) with docetaxel was more effective than monotherapy, lowering LGR5 levels and suppressing tumor growth. In summary, there is a functional link between AURKA and LGR5, mediated by STAMBP to promote stem-like properties and enhance cell survival in gastric tumorigenesis. Targeting the AURKA-LGR5 axis is a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/07/11
Gomaa AhmedMaacha SelmaSoutto MohammedGiordano SilviaBhat NadeemKumar ShriaMcDonald Oliver GEl-Rifai Wael - Transcription activation of genes by estrogen is driven by enhancers, which are often located within the same topologically associating domain (TAD) as non-targeted promoters. We investigated how acute enhancer-driven activation affects neighbouring non-target genes within the same TAD. Using single-molecule RNA FISH (smFISH), we tracked the transcription of TFF1 (enhancer-target gene) and TFF3 (non-target gene) during estrogen stimulation. We observed mutually exclusive expression patterns: TFF1 expression peaked at 1 hr, while TFF3 reached its peak at 3 hr after TFF1 activation had diminished. Chromatin looping data indicated that the enhancer loops with the TFF1 gene but not TFF3, suggesting that TFF3 upregulation is not due to direct enhancer-promoter interactions. CRISPR deletion of the enhancer affected TFF1 transcription more acutely than TFF3. 1,6-hexanediol (HD) exposure suggested that the TFF1 enhancer:promoter undergoes a potential ERα-mediated condensate formation, which sequesters the transcriptional machinery and inhibits TFF3 expression. As estrogen signaling fades at 3 hr, TFF1 expression declines while TFF3 expression increases. Our findings reveal that enhancer-driven activation can indirectly repress neighboring genes within the same TAD, highlighting a dynamic shift in gene expression as signaling progresses. - Source: PubMed
Publication date: 2026/07/07
Bohra DarshikaIslam ZubairulNidharshan SundarrajMazumder AprotimNotani Dimple