AKR1C3 antibody
- Known as:
- AKR1C3 (anti-)
- Catalog number:
- orb29630
- Product Quantity:
- 5 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- AKR1C3 antibody
Related genes to: AKR1C3 antibody
- 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 antibody
Related articles to: AKR1C3 antibody
- Hyperandrogenism during childhood is a key feature of several pediatric endocrine disorders, including premature adrenarche and polycystic ovary syndrome (PCOS). The adrenal gland contributes significantly to circulating androgens, yet the regulation of adrenal steroidogenic enzymes during the prepubertal period remains poorly understood. This study aimed to investigate adrenal androgen synthesis in a prepubertal rat model of ovarian removal and identify key enzymes responsible for hyperandrogenism. - Source: PubMed
Publication date: 2026/05/27
Gao GuanglinWang JunqiZhan BowenLi BowenShao YanyanHan XinghuiHe JingweiSun WenYu JianDong Wenke - Aldo-keto reductase family 1 member C3 (AKR1C3) is a pivotal metabolic enzyme involved in arachidonic acid (AA) metabolism and cancer metabolic reprogramming, which plays a critical role in the initiation and progression of glioblastoma (GBM). We integrated single-cell and transcriptome data to characterize AA metabolism features in GBM and identify the key gene AKR1C3. Using CCK8 assays, wound-healing assays, transwell assays, and mouse tumor formation experiments, we elucidated the effects of AKR1C3. Dual-luciferase reporter assays and ChIP-PCR experiments were performed to investigate the regulation of transcription factor JUN on AKR1C3 expression. RNA-seq analysis, combined with rescue experiments, demonstrated that AKR1C3 significantly regulates the RhoA/ROCK pathway. Arachidonic acid metabolism is closely associated with clinical outcomes in glioma, with AKR1C3 identified as a key gene within this pathway. AKR1C3 knockdown enhanced tumor cell proliferation, migration, and invasion, whereas AKR1C3 overexpression suppressed these malignant behaviors. In vivo experiments further confirmed the inhibitory effect of AKR1C3 on glioma progression. Dual-luciferase reporter and ChIP-PCR assays demonstrated that JUN acts as an upstream regulator of AKR1C3. ELISA results indicated that AKR1C3 overexpression reduced cellular PGD2 levels. RNA-seq analysis suggested that the RhoA/ROCK pathway was a downstream effector of AKR1C3, and exogenous PGD2 supplementation could reverse AKR1C3-mediated regulation of this pathway. We identified curcumin, a natural product with anti-cancer metabolic regulatory activity, as an upstream modulator that suppresses JUN expression, thereby activating the JUN/AKR1C3 axis and inhibiting malignant phenotypes in GBM cells. JUN/AKR1C3 axis influences glioma progression via modulating PGD2-mediated RhoA/ROCK Signaling. - Source: PubMed
Publication date: 2026/07/03
Wang JieMa HuihaoFeng BaozhiFu YanLu ChunlinFei MingyangZhang YuxinDong BinLi YingLiu Jing - Aldo-keto reductase 1C3 (AKR1C3) is a drug target for the treatment of various androgen dependent malignancies, including castration-resistant prostate canceras well as hematological cancers. The enzyme plays a key role in the conversion of androgen precursors into potent androgen receptor ligands and the conversion of prostaglandins from pro-differential to pro-proliferative, facilitating progression of these malignancies. Additionally, AKR1C3 plays a role in chemotherapy resistance, reducing therapeutics to inactive forms and stabilizing expression of mutant androgen receptors. - Source: PubMed
Publication date: 2026/07/03
Case Alfie MSmith Melanie MMack Cole ATrippier Paul C - OBI-3424 is an investigational small molecule prodrug. In a dose-escalation trial, the OBI-3424 recommended phase 2 dose (RP2D) was 12 mg/m2 administered every 21 days. In this phase 2 dose-expansion trial, we evaluated the safety and efficacy of OBI-3424 in pancreatic adenocarcinoma and other solid tumor types ("basket" cohort). - Source: PubMed
Publication date: 2026/07/02
Tsimberidou Apostolia MariaVerschraegen ClaireSigal DarrenLenz Heinz-JosefHochster HowardBaysal Mehmet AChakraborty AbhijitLee InglyRistoski KoenuelXu Dong - Castration-resistant prostate cancer (CRPC) is a lethal stage of prostate cancer (PC). This research sought to examine the functions and underlying mechanisms of N-methyladenosine (mA) methyltransferases in CRPC. Transcriptomic datasets from the Gene Expression Omnibus and The Cancer Genome Atlas were analyzed to identify dysregulated mA methyltransferases. Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine incorporation, wound healing, Transwell, enzyme-linked immunosorbent assay, reverse transcription quantitative polymerase chain reaction, western blot, mA RNA immunoprecipitation quantitative PCR, co-immunoprecipitation, and mA quantification assays were performed to evaluate the phenotypic and molecular effects of methyltransferase-like 3 (METTL3). A xenograft tumor model was constructed by subcutaneous injection of lentivirus-transduced LNCaP cells into BALB/c nude mice. Hematoxylin and eosin staining was utilized to detect histopathological alterations, and immunohistochemistry was applied to measure Ki67 expression. METTL3 and methyltransferase-like 5 were upregulated, whereas methyltransferase-like 4 was downregulated. METTL3 knockdown suppressed the proliferation, migration, invasion, and epithelial-mesenchymal transition in LNCaP and C4-2 cells and suppressed xenograft tumor growth. METTL3 knockdown reduced dihydrotestosterone production and suppressed the protein expression of androgen receptor, kallikrein-related peptidase 3, and FK506 binding protein 5. METTL3 enhanced the mA methylation and transcript stability of aldo-keto reductase family 1 member C3 (AKR1C3). AKR1C3 overexpression notably reversed the anti-tumor effects induced by METTL3 knockdown. METTL3 acts as an epigenetic driver of CRPC by promoting AKR1C3 expression in an mA-dependent manner, highlighting the METTL3/AKR1C3 axis as a promising treatment target. - Source: PubMed
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