FasL (tet_on)
- Known as:
- FasL (tet_on)
- Catalog number:
- 000134A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FasL (tet_on)
Related genes to: FasL (tet_on)
- Gene:
- FASLG NIH gene
- Name:
- Fas ligand
- Previous symbol:
- APT1LG1, TNFSF6
- Synonyms:
- FasL, CD178
- Chromosome:
- 1q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-09
- Date modifiied:
- 2019-04-23
Related products to: FasL (tet_on)
Related articles to: FasL (tet_on)
- Upper tract urothelial carcinoma (UTUC) is characterized by a high incidence of muscle invasion and distinct molecular heterogeneity, with tumor microenvironment (TME) heterogeneity playing a pivotal role in its malignant progression. However, the spatial distribution patterns of functional cell populations in UTUC and their regulatory mechanisms driving high-grade (HG) and muscle-invasive (MI) progression remain largely unelucidated. Herein, we integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptome sequencing (ST-seq) to systematically characterize the cellular landscape, spatial molecular network, and intercellular communication profile of UTUC tissues. Six tumor cell subpopulations were identified in UTUC, among which SLC14A1⁺ tumor cells were correlated with favorable clinical prognosis, whereas S100A8/9⁺ tumor cells were associated with poor clinical outcomes. Mechanistically, SLC14A1⁺ tumor cells decelerated UTUC progression via modulating cell apoptosis mediated by the FASLG-TNFRSF10B ligand-receptor pair. In contrast, S100A8/9⁺ tumor cells promoted the malignant progression of UTUC by regulating extracellular matrix remodeling and epithelial-mesenchymal transition (EMT) via the CCL19-CCR7, CCN2-EGFR, ADAM28-ITGA4 and CD14-ITGB2 ligand-receptor pairs. Collectively, our study uncovers the cellular and spatial heterogeneity of the UTUC TME, identifies SLC14A1⁺ tumor cells as a tumor-suppressive subpopulation and S100A8/9⁺ tumor cells as a key driver of UTUC malignant progression, and further delineates the core spatial signaling pathways underlying HG and MI progression of UTUC. These findings provide novel prognostic biomarkers and potential therapeutic targets for UTUC, and advance our mechanistic understanding of spatial TME regulation in urothelial carcinoma. - Source: PubMed
Publication date: 2026/09/03
Liu JiangWei YangyangLiu YiSun ShiweiDilixiati DiliyaerZhou ZhouLu XiangyunLu PingZhao YangZhang YuShi - One of the key hallmarks of aging is the age-related decline in immune system function, accompanied by a chronic low-grade inflammation, or "inflammaging". Simultaneously, a reduced capacity of immune cells to recognize and eliminate pathogens, along with immune exhaustion, is also defined as a sign of aging. Cynomolgus macaques () belong to a group of non-human primates evolutionarily close to humans and are often used for preclinical research. - Source: PubMed
Publication date: 2026/08/13
Petrova Viktoria MBulgin Dmitry VRadomskaya Elena YuShevelov Vsevolod AZhukova Darya SChzhu Olga PManakhov Andrey DPopov Alexander VRybtsov Stanislav A - Photodynamic priming (PDP), a fallout of photodynamic therapy, transiently modulates the tumor microenvironment (TME), enhances therapeutic susceptibility, and promotes immunogenic cell death through the release of damage-associated molecular patterns (DAMPs). Pancreatic ductal adenocarcinoma (PDAC) remains non-responsive to current therapies with a desmoplastic and immunosuppressive TME that limits drug delivery and blunts responses to immune checkpoint blockade. We investigated whether PDP could enhance anti-PD1 therapy responses in PDAC using patient-derived organoids (PDOs). PDOs were treated with Visudyne and red light (25, 75, and 100 J/cm²), followed by assessment of cytotoxicity, DAMP expression (HSP60, calreticulin, HMGB1), and transcriptomic changes. Monocyte-derived dendritic cells (mDCs) from healthy donors were cocultured with PDP-treated (25 J/cm) PDOs, then with matched naïve T cells. mDC and T cell activation markers were analyzed. Pembrolizumab (anti-PD1) was added to PDO-mDC-T cell cocultures to evaluate combined effects on PDO viability and T cell activation. PDP induced dose-dependent cytotoxicity and upregulated DAMPs. Gene profiling in PDOs showed increased , , and , with reduced , , and expression. mDCs exposed to PDP-treated PDOs upregulated CD40, CD86, and MHC-II, driving activation of CD4 and CD8 T cells, evidenced by elevated PD1 expression. Addition of pembrolizumab further decreased PDO viability and amplified effector cytokines (, , , B, , ). PDP was associated with modulation of the PDAC TME toward a more immunogenic phenotype by enhancing tumor immunogenicity, activating dendritic cells and T cells, and potentiating PD1 blockade. These findings provide mechanistic support for further preclinical and clinical evaluation of PDP combined with checkpoint inhibition in PDAC. - Source: PubMed
Publication date: 2026/08/11
De Silva PushpamaliWekking DemiChoe Joanna JoeunKidd Madeline DPearce Josie LRocha Castellanos Dario MissaelZelga PiotrJenkins RussellWang Kenneth KChandrasekhara VinayMaytin Edward VLiss Andrew ScottHasan Tayyaba - Colorectal cancer (CRC) remains a major global health burden, while current therapeutic strategies are often constrained by limited efficacy and adverse side effects. This study evaluated the anticancer activity and DNA-binding properties of a novel platinum-Mesalazine complex (Pt-MES) compared with Mesalazine (MES) in human CRC cells. Cytotoxicity was assessed using the MTT assay, gene expression was analyzed by qPCR, and drug-DNA interactions were investigated through viscosimetry, UV-visible spectroscopy, and molecular docking. Both compounds exhibited dose-dependent cytotoxicity; however, Pt-MES demonstrated superior antiproliferative activity, with a lower IC₅₀ value (2.694 µg/mL) than MES (3.503 µg/mL), indicating enhanced efficacy following platinum complexation. Gene expression analysis revealed that Pt-MES promoted apoptosis by upregulating FASLG, BAX, and miRNA-122, while suppressing Bcl-2, telomerase, and miRNA-21. In contrast, MES exerted weaker regulatory effects on these molecular targets. Biophysical studies showed a slight reduction in DNA viscosity accompanied by hyperchromic shifts in UV-visible spectra, suggesting a predominantly non-intercalative mode of DNA interaction. Molecular docking further supported preferential binding within the DNA minor groove. These findings indicate that Pt-MES may interact with DNA grooves and facilitate platinum coordination with nucleophilic sites, particularly guanine residues, leading to DNA structural perturbation and activation of apoptotic pathways. In addition, Pt-MES may influence key pathways implicated in CRC progression, including NF-κB, Wnt/β-catenin, and COX-2 signaling. Collectively, the results demonstrate that Pt-MES exhibits enhanced in vitro anticancer activity relative to MES and represents a promising multi-targeted candidate for further preclinical investigation in colorectal cancer. - Source: PubMed
Publication date: 2026/08/09
Ghasemi KimiyaSabokrouh AbdolrezaNoohi BahareModarresi Farrokh - - Source: PubMed
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