CD178 _ Fas Ligand
- Known as:
- CD178 _ Fas Ligand
- Catalog number:
- GTX100644
- Product Quantity:
- 100 µl
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD178 _ Fas Ligand
Ask about this productRelated genes to: CD178 _ Fas Ligand
- 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
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&_945;2&_946;1 Integrin Ligand Peptide(1R,2R)_(+)_1,2_Diaminocyclohexane_N, min. 94%rost ligand (na(1S,2S)_(+)_1,2_Cyclohexanediamino_N, (S,S)_Jacobsen ligand(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N min. 94% rost ligand (n(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N Rost ligand24(S)-Hydroxycholesterol Ligand24(S)-Hydroxycholesterol Ligand24(S)-Hydroxycholesterol, LXR ligand, (3β,24S)-Cholest-5-ene-3,24-diol, CAS: 474-73-724(S)-Hydroxycholesterol, LXR ligand, (3β,24S)-Cholest-5-ene-3,24-diol, CAS: 474-73-72B4,CD244,h2B4,Homo sapiens,Human,NAIL,Natural killer cell receptor 2B4,NK cell activation-inducing ligand,NK cell type I receptor protein 2B4,NKR2B42C101 Fas Ligand2R2 Fas3.22 Fas- FITC labeled3.22 Fas-PE labeled3D5 Fas Death Domain Related articles to: CD178 _ Fas Ligand
- 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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Publication date: 2026/07/06
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