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)
- Late occurrence of breast cancer brain metastases in patients pretreated with systemic therapies is often associated with therapy resistant brain metastatic lesions. Prior studies targeting previously identified mediators of resistance have yielded limited success, especially in the case of brain metastatic breast cancer (BMBC). Trefoil Factor 1 (TFF1) has been associated with therapy resistance in Estrogen Receptor (ER) positive breast cancer. However, its role in therapy resistance of triple negative and HER2+ breast cancer remains elusive. Herein, we assessed the involvement of TFF1 in therapy resistant triple negative and HER2+ BMBC. We developed Paclitaxel resistant triple negative and Lapatinib resistant HER2+ BMBC cells by dose escalation method. Drug efflux transporter ABCB1 in Paclitaxel resistant cells and ABCG2 in Lapatinib resistant cells were significantly upregulated. Additionally, cancer stem cell marker, CD24, showed significant upregulation in both resistant cell lines while anti-apoptotic protein BCL2 was upregulated only in Lapatinib resistant cells. Importantly, TFF1 was significantly upregulated in both Paclitaxel and Lapatinib resistant BMBC cells. Moreover, siRNA mediated TFF1 silencing partially alleviated resistance in both Paclitaxel and Lapatinib resistant BMBC cells. Our study shows that TFF1 is potentially associated with resistance to Paclitaxel and Lapatinib in both triple negative and HER2+ BMBC. - Source: PubMed
Publication date: 2026/09/28
Gurung Sumiran KumarYakati VenuKondapaneni Raghu VamsiShevde Lalita ARao Shreyas - Diethyl phthalate (DEP) is commonly used in cosmetics, personal care products, and pharmaceutical formulations as a low-molecular-weight phthalate. Despite its widespread use, information on its effects on the gastric mucosa remains limited. This study examined the dose-related effects of DEP on inflammation, oxidative stress, gastric mucosal defense, DNA damage, apoptosis, and histopathological changes in rat gastric tissue. Twenty-eight female Wistar rats were randomly assigned to four groups (n = 7 per group): control and DEP (100, 300, or 600 mg/kg/day). These experimental toxicological doses were administered by oral gavage for 21 days. Gastric tissue levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), superoxide dismutase (SOD), malondialdehyde (MDA), trefoil factor family 1 (TFF1), and mucin-5AC (MUC5AC) were determined by ELISA. Histopathological examination, Bax/Bcl-2 immunohistochemistry, and comet assay were performed. Dose-response relationships were assessed using polynomial trend analysis. DEP exposure resulted in significant dose-dependent increases in IL-6, TNF-α, COX-2, MDA, Bax expression, Bax/Bcl-2 ratio, histopathological damage, and DNA damage (all p < 0.001), whereas SOD levels and Bcl-2 expression significantly decreased (all p < 0.001). TFF1 and MUC5AC levels were significantly increased at 100 mg/kg but significantly decreased at 600 mg/kg compared with controls. Histopathological examination showed progressive gastric mucosal injury with increasing DEP doses. DEP exposure induced dose-related changes in gastric inflammation, oxidative stress, mucosal protective factors, histopathology, DNA damage, and apoptosis-related protein expression. The findings suggest that oxidative stress and inflammation are associated with altered mucosal defense, DNA damage, and apoptosis following DEP exposure. - Source: PubMed
Publication date: 2026/09/17
Gokdemir Gul SahikaYavaş Mehmet CihanDemirtaş SelimTan Fazile CantürkVarol SalihGokdemir Mehmet Tahir - Invasive mucinous adenocarcinoma (IMA) of the lung is a distinct subtype of lung adenocarcinoma with unique clinicopathologic features; however, its histogenesis remains incompletely understood. Although mucinous metaplasia has been suspected as a precursor lesion, direct molecular evidence supporting this progression is limited. In this study, we applied morphology-guided spatial transcriptomics to investigate epithelial lineage relationships across the mucinous spectrum of lung lesions. Formalin-fixed, paraffin-embedded lung tissues from 26 patients were analyzed using the GeoMx digital spatial profiling platform. A total of 118 cytokeratin-positive regions of interest representing normal bronchioles, bronchiolar metaplasia, mucinous metaplasia, mucinous dysplasia, IMA, nonmucinous terminal respiratory unit-type adenocarcinoma, squamous metaplasia/dysplasia, and squamous cell carcinoma were profiled. Spatial transcriptomic data were integrated with two independent public cohorts and mapped to the Human Lung Cell Atlas for epithelial cell-type assignment. Unsupervised clustering identified a distinct mucinous cluster comprising IMA and most mucinous dysplasia regions, characterized by enrichment of gastric-type differentiation markers, including MUC5AC, MUC6, TFF1, TFF2, and CLDN18. Label-transfer analysis demonstrated that mucinous metaplasia and dysplasia were predominantly associated with club and goblet cell identities, whereas IMAs showed enrichment of club and goblet signatures. In contrast, nonmucinous adenocarcinomas consistently aligned with alveolar type 2 cell identity across all datasets. Immunohistochemistry confirmed uniform CLDN18 expression in IMAs and its absence in nonmucinous adenocarcinomas. These findings provide spatial transcriptomic evidence supporting a club cell-associated mucinous pathway in lung tumorigenesis and identify CLDN18 as a defining molecular feature of IMA. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/09/08
Park Joon YoungKim Do YeonLee Hyun JungLee Jung HeePark Hae RyounShin Dong Hoon - Transcriptional bursts regulate gene expression by altering burst size or burst frequency. Here, we present a protocol to analyze estrogen-responsive transcriptional bursting of the TFF1 gene in human breast cancer cell lines by integrating fixed-cell single-molecule RNA fluorescence in situ hybridization (smFISH) and live-cell single-molecule imaging. We describe cell seeding, ligand dose-response treatment, and smFISH hybridization and imaging to quantify transcription sites. We then detail live-cell imaging of a TFF1-MS2 reporter and integration of both datasets to resolve how endocrine disruptors modulate bursting dynamics. For complete details on the use and execution of this protocol, please refer to Day et al.. - Source: PubMed
Publication date: 2026/09/08
Yaşar PelinDay Christopher RRodriguez Joseph - Neutrophil extracellular trap-driven necrosis-related genes (NRGs) and inflammation-related genes (IRGs) are crucial in mitigating or inhibiting cancer progression in breast cancer patients. The interaction between NRGs and IRGs in breast cancer remains unclear. Thus, identifying prognostic genes associated with NETosis and inflammation in breast cancer may offer a novel approach to improving the outcome of breast cancer. - Source: PubMed
Publication date: 2026/08/21
Xu ZhihongMa QianJiang QihuaWei WensongTao Dan