AKR1C3 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- AKR1C3 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00008644-T02
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AKR1C3 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: AKR1C3 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
Related products to: AKR1C3 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: AKR1C3 293T Cell Transient Overexpression Lysate(Denatured)
- Triphala is a traditional three-fruit formulation with potential anticancer activity, but its ferroptosis-related mechanisms in oral cancer remain unclear. We integrated network pharmacology, transcriptomic analyses, prognostic modeling, Mendelian randomization, immune and drug-response analyses, molecular docking, and in vitro validation to investigate the Triphala-ferroptosis-oral cancer axis. Fifty-eight candidate functional genes were identified, and an eight-gene signature comprising AKR1C3, CA9, EGFR, GSTA1, MAPK8, MGST1, PPARG, and RB1 showed prognostic value across multiple cohorts. Mendelian randomization supported causal associations of MAPK8, MGST1, and PPARG with oral cancer risk. Seven Triphala-derived compounds, including epigallocatechin gallate, quercetin, kaempferol, luteolin, ellagic acid, gallic acid, and quinine, displayed favorable predicted interactions with key targets. In CAL-27 cells, Triphala altered the expression of signature genes, reduced GPX4 and SLC7A11 protein levels, increased Feand malondialdehyde, depleted glutathione and glutathione peroxidase activity, and enhanced lipid peroxidation; these effects were partially modulated by ferrostatin-1. This study advances the field by linking Triphala to a ferroptosis-based prognostic framework and experimentally demonstrating its regulation of the SLC7A11-GSH-GPX4 axis in oral cancer. - Source: PubMed
Zhao YiweiLi SiminJiang LinxinKreher DeborahSchmalz GerhardFichter AndreasHu Xianda - Globally, myocardial infarction (MI) remains a major cause of morbidity and mortality. Macrophage-mediated inflammation and ferroptosis-related stress responses have both been implicated in MI; however, transcriptomic identification of macrophage- and ferroptosis-related candidate genes requires rigorous control of false-positive findings. In this revised study, two peripheral blood transcriptomic datasets, GSE29532 and GSE48060, were integrated after probe annotation, independent normalization, merging based on common genes, and ComBat batch correction. Batch-correction quality was evaluated using both visualization and quantitative metrics. Differential expression analysis was performed using the limma package with adj.P.Val < 0.05 as the primary threshold. A total of 213 differentially expressed genes were identified, including 101 upregulated and 112 downregulated genes. Intersecting FDR-supported DEGs with macrophage-related and ferroptosis-related gene sets identified seven primary MFRDEGs: SMAD7, MMD, PTPN6, DDIT3, AKR1C3, PHF21A, and ACSL1. GO enrichment analysis was interpreted as exploratory functional annotation because of the small input gene set, whereas whole-ranked-gene GSEA highlighted TNFA/NF-kB inflammatory signaling, complement-related innate immune signaling, and reactive oxygen species-related transcriptional programs. Because the revised PPI analysis did not produce reliable interactions among the seven primary MFRDEGs, candidate gene prioritization was performed instead of defining interaction-derived hub genes. ssGSEA suggested a robust neutrophil-related alteration in MI, while macrophage- and monocyte-related signatures showed trend-level changes after FDR correction. Exploratory ROC analysis was performed for selected candidate genes. RT-qPCR validation further showed that SMAD7, PTPN6, DDIT3, PHF21A, and ACSL1 were increased, whereas MMD and AKR1C3 were decreased in AMI peripheral blood samples, consistent with the transcriptomic results. These findings provide FDR-supported candidate-level evidence linking macrophage- and ferroptosis-related transcriptional alterations to immune signatures in MI and warrant further validation in larger cohorts and mechanistic studies. - Source: PubMed
Publication date: 2026/08/25
Wang GuoqinZhang ZhulinYang GuanruiWang JingMa TengGuo Shuang - Cigarette smoking is associated with a poor prognosis and reduced efficacy of androgen receptor signaling inhibitors (ARSIs) in prostate cancer patients; however, the underlying molecular mechanisms remain largely undefined. This study investigated the impact of cotinine, the stable primary metabolite of nicotine, on androgen-dependent growth and therapeutic sensitivity in human prostate cancer 22Rv1 cells. While cotinine alone did not affect basal prostate-specific antigen (PSA) levels, it significantly potentiated 5α-androstane-3,17-dione (5α-Adione)-induced PSA expression and cell proliferation. Mechanistic investigations revealed that cotinine did not modulate the expression levels of androgen-synthesizing enzymes (e.g., AKR1C3, DHRS11) and E3 ubiquitin ligases. Instead, cotinine significantly extended the protein half-life of both the full-length androgen receptor (AR) and the constitutively active splice variant AR-V7. Co-immunoprecipitation assays indicated that cotinine increased the association between AR and the molecular chaperone HSP70, thereby protecting AR proteins from ubiquitin-proteasome-mediated degradation. Collectively, these findings provide a molecular basis for the adverse clinical outcomes observed in smokers, suggesting that the accumulation of cotinine may serve as a potential risk factor for prostate cancer progression and treatment resistance. - Source: PubMed
Publication date: 2026/08/19
Hayashi RiriKudo YudaiYoshino YutaShiota MasakiFujimoto NaohiroIkari AkiraEndo Satoshi - Myxoglucamides, natural products recently isolated from Cystobacterineae sp., are featured by an unprecedented vinyl-substituted α-keto-γ-amino acid that is linked to a glycosylated 14-methyl-pentadecanoic acid. Thus, they unite elements from three biomolecular classes in a compact glycolipopeptide. To elucidate the biological relevance of this arrangement, we searched for molecular targets by activity-based protein profiling (ABPP)-although a phenotypic bioactivity has not been reported. An access to the compound class was established through the first total synthesis of myxoglucamide A in 11 steps. A proteome-wide ABPP study led to the identification of aldo-keto reductase 1C3 (AKR1C3) as the primary target of myxoglucamides in human cells. AKR1C3 is an oncogenic factor involved in prostaglandin and steroid synthesis, promoting the growth, proliferation, and metastasis of carcinoma cells. The functional inhibition of AKR1C3 by a competitive mechanism (IC = 1.61 µm) was validated in vitro, and 20 analogs provided structure-activity relationships and more potent analogs (IC = 181 nm). Biophysical interactions were quantified by thermal shift assays, and essential molecular protein-ligand interactions were characterized by X-ray crystallography at 2.0 Å resolution. The study implies that the search for targets of natural products is rewarding even in the absence of an initial phenotypic activity. - Source: PubMed
Publication date: 2026/08/10
Siemon ThomasMishra Vivek KZhao MingmingBüssow KonradPopoff AlexanderFu ChengzhangMüller RolfJänsch LotharBlankenfeldt WulfBrönstrup Mark - This study investigated the preliminary role of γ-oryzanol (γ-O) against breast cancer through computational and in vitro analyses. Reference protein set (RPS) and functional enrichment set (FES) proteins were identified and subjected to network pharmacology. Pharmacogenomics analysis assessed expression profiles and survival associations. Molecular docking of γ-O with PIK3CA, AKT1, AKR1C3, ESR1, and MAPK1 was performed, followed by molecular dynamics (MD) simulation of the γ-O-PIK3CA complex. Brine shrimp lethality assay (BSLA) evaluated the effect of γ-O on nauplii survival and percentage lethality. Allium cepa root tip assay (ACARTA) assessed the effect of γ-O in number and length of roots. Cell viability assay evaluated MCF-7 cell viability after γ-O treatment. Target validation and network pharmacology suggested the relevance of RPS and FES with cancer-associated pathways. Pharmacogenomics analysis highlighted FES overexpression with reduced survival associations and cancer progression. Molecular docking predicted interaction of γ-O with PIK3CA (- 9.1 kcal/mol), AKT1 (- 7.2 kcal/mol), AKR1C3 (- 12.3 kcal/mol), ESR1 (- 8.3 kcal/mol), and MAPK1 (- 8.9 kcal/mol). MD simulation indicated the stability of γ-O-PIK3CA complex. γ-O treatment significantly (P-value < 0.05) reduced nauplii survival and increased percentage lethality. The number and length of roots reduced significantly (P-value < 0.05) in γ-O-treated roots. γ-O produced a significant (P-value < 0.05) concentration-dependent reduction in cell viability (half-maximal inhibitory concentration = 352.57 ± 48.51 µg/mL). BSLA, ACRTA, and cell viability assay demonstrated preliminary cytotoxic, anti-mitotic, and anti-proliferative effects of γ-O, aligned with computational target and interaction analyses. Further studies are required to validate its mechanistic relevance against breast cancer. - Source: PubMed
Publication date: 2026/07/29
Sukhadia MahimaPatel HoneyGupta AdarshJawarkar RahulShah UmangPatel AlkeshkumarRaval Keval