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更新于：2025-05-07

AKR1C1

更新于：2025-05-07

基本信息

别名

20-alpha-HSD、20-alpha-hydroxysteroid dehydrogenase、AKR1C1

+ [10]

简介

Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids (PubMed:19218247). Most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentrations of NADPH (PubMed:14672942). Displays a broad positional specificity acting on positions 3, 17 and 20 of steroids and regulates the metabolism of hormones like estrogens and androgens (PubMed:10998348). May also reduce conjugated steroids such as 5alpha-dihydrotestosterone sulfate (PubMed:19218247). Displays affinity for bile acids (PubMed:8486699).

关联

靶点

AKR1C1

作用机制

AKR1C1 inhibitors

在研机构-

原研机构

Monash Institute of Pharmaceutical Sciences

在研适应症-

非在研适应症

肿瘤 [+1]

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 AKR1C1 相关的临床结果

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100 项与 AKR1C1 相关的转化医学

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0 项与 AKR1C1 相关的专利（医药）

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662

项与 AKR1C1 相关的文献（医药）

2025-04-01·European Journal of Clinical Microbiology & Infectious Diseases

The first two human infections with Helicobacter zhangjianzhongii, a new Helicobacter closely related to Helicobacter canis

Article

作者: Wandji, Sahel ; Lehours, Philippe ; Jehanne, Quentin ; Jauvain, Marine ; Bénéjat, Lucie ; Levast, Marion ; Ducournau, Astrid ; Aptel, Johanna

PURPOSEIn 2023, Helicobacter zhangjianzhongii was proposed as a new species in the Helicobacter genus. We here describe two human cases of H. zhangjianzhongii bacteremia.METHODSFour clinical strains from the Helicobacter genus isolated from blood culture between 2017 and 2023 were studied. They were initially identified as H. canis by MALDI-TOF and 16S rDNA sequencing. The strains were biochemically characterized and tested at different temperatures and atmospheres. Two databases were used to characterize the isolates: the Bruker® MBT compass Version 4.1.1 database and a in-house spectrum-enriched database. After bacterial DNA extraction the genomes were sequenced on NovaSeq 6000 (Illumina) and analyzed using an in-house pipeline.RESULTSCase 1 involved a 58-year-old woman who was hospitalized in a thoracic oncology unit because her general condition deteriorated in a setting of small-cell carcinoma. She presented with abdominal pain associated with significant hepatomegaly. Case 2 involved a 78-year-old woman on rituximab who was hospitalized to treat chest pain, anemia, and inflammatory syndrome. Both strains exhibited very similar microbiological and genomic characteristics, thus growth in a microaerobic atmosphere at 37°C and 42°C, oxidase-positivity, and urease- and catalase-negativity. Both were formally identified by whole-genome sequencing as H. zhangjianzhongii (ANI > 99% and DDH > 94%).CONCLUSIONThis proposed species is associated with bacteremia in humans. It is thus likely to be a novel human pathogen. Dogs may have been the source of infection.

2025-04-01·Biological Research For Nursing

Preterm Birth in African American Women: A Multi-Omic Pilot Study in Early Pregnancy

Article

作者: Liang, Xiaoyu ; Zhang, Wei ; Misra, Dawn P. ; Woo, Jennifer ; Anderson, Cindy M. ; Saadat, Nadia ; Forsman, Anna M. ; Engeland, Christopher G. ; Sun, Jiao ; Giurgescu, Carmen ; Joyce, Cara ; Nowak, Alexandra L.

Preterm birth (PTB; <37 weeks completed gestation) is a devastating problem affecting over 13 million live births worldwide. In the U.S., African Americans experience significantly higher rates of PTB compared to non-Hispanic Whites. PTB disparities have been linked to social determinants of health (e.g., socioeconomic status, discrimination). However, the biological underpinnings related to these associations are unclear. DNA methylation (DNAm) is subject to environmental influences, and DNAm modifications are known to affect gene expression. Using a multi-omic approach, we examined differences in combined DNA methylation (DNAm) and messenger RNA (mRNA) transcriptomic data from 20 pregnant African American women (12 PTB; 8 term birth) early in pregnancy (8–18 weeks gestation). We found that the HLA- DQB2 gene was both differentially methylated (cg12296550; p = .02) and differentially expressed ( p = .014; log2FC = 2.5) between women with PTB and term birth. Gene expression analysis showed HLA- DQB2 and HLA- DRB4 ( p = .028; log2FC = −3.6) were the two most highly expressed genes. HLA-DQB2 expressed higher in PTB and HLA- DRB4 expressed higher in term birth. However, no genes remained significant ( p < .05) after Bonferroni correction. HLA- DRB4 and AKR1C1 were identified as a potential biomarkers in dimensionality reduction models and are also important to immune function and allogenic breakdown. Altered gene expression may lead to inflammatory imbalances or allogenic intolerance resulting in PTB. This study provides proof-of-concept evidence for the feasibility and importance of future multi-omics studies with larger populations to further explore the genes and pathways identified here.

2025-03-01·Cell Death & Differentiation

The AKR1C1–CYP1B1–cAMP signaling axis controls tumorigenicity and ferroptosis susceptibility of extrahepatic cholangiocarcinoma

Article

作者: Zhao, Zhibin ; Gao, Minghui ; Zhou, Lin ; Yu, Wenlong ; Liu, Chang ; Wang, Zhenhua ; Yang, Jieli ; Lian, Zhexiong ; Wu, Hongkun ; Zhang, Xiaomin ; Zhang, Cheng

AbstractExtrahepatic cholangiocarcinoma (ECC), a highly malignant type of cancer with increasing incidence, has a poor prognosis due to limited treatment options. Based on genomic analysis of ECC patient samples, here we report that aldo-keto reductase family 1 member C1 (AKR1C1) is highly expressed in human ECC tissues and closely associated with ECC progression and poor prognosis. Intriguingly, we show that inducible AKR1C1 knockdown triggers ECC cells to undergo ferroptosis. Mechanistically, AKR1C1 degrades the protein stability of the cytochrome P450 family member CYP1B1, a newly discovered mediator of ferroptosis, via ubiquitin-proteasomal degradation. Additionally, AKR1C1 decreases CYP1B1 mRNA level through the transcriptional factor aryl-hydrocarbon receptor (AHR). Furthermore, the AKR1C1–CYP1B1 axis modulates ferroptosis in ECC cells via the cAMP–PKA signaling pathway. Finally, in a xenograft mouse model of ECC, AKR1C1 depletion sensitizes cancer cells to ferroptosis and synergizes with ferroptosis inducers to suppress tumor growth. Therefore, the AKR1C1–CYP1B1–cAMP signaling axis is a promising therapeutic target for ECC treatment, especially in combination with ferroptosis inducers.

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