^
Contact us  to learn more about
our Premium Content:  News alerts, weekly reports and conference planners
BIOMARKER:

AKR1C3 overexpression

i
Other names: AKR1C3, Aldo-Keto Reductase Family 1 Member C3, Prostaglandin F Synthase, Trans-1,2-Dihydrobenzene-1,2-Diol Dehydrogenase, 3-Alpha Hydroxysteroid Dehydrogenase, Type II, Testosterone 17-Beta-Dehydrogenase 5, Chlordecone Reductase Homolog HAKRb, Dihydrodiol Dehydrogenase X, Dihydrodiol Dehydrogenase 3, 3-Alpha-HSD Type II, Brain, Indanol Dehydrogenase, HSD17B5, HAKRB, Aldo-Keto Reductase Family 1, Member C3 (3-Alpha Hydroxysteroid Dehydrogenase, Type II), Type IIb 3-Alpha Hydroxysteroid Dehydroge
Entrez ID:
Related biomarkers:
6ms
Radiotherapy Resistance in Prostate Cancer Cells: AKR1C3 Inhibition of Ubiquitinated Degradation of Nrf2 through Interaction with KEAP1. (PubMed, Int J Radiat Oncol Biol Phys)
In sum, we found that AKR1C3 can bind with Keap1 leading to reduced ubiquitination level of Nrf2, causing upregulation of Nrf2 expression and providing new insights into PCa radiotherapy resistance.
Journal
|
KEAP1 (Kelch Like ECH Associated Protein 1) • NFE2L2 (Nuclear Factor, Erythroid 2 Like 2) • AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression • AKR1C3 expression
|
MG132
8ms
Aldo-Keto Reductase 1C3 Inhibitor Prodrug Improves Pharmacokinetic Profile and Demonstrates In Vivo Efficacy in a Prostate Cancer Xenograft Model. (PubMed, J Med Chem)
The in vivo pharmacokinetic evaluation revealed an increase in systemic exposure and increased the maximum 5r concentration compared to direct administration of the free acid. The prodrug 4r demonstrated a dose-dependent effect to reduce the tumor volume of 22Rv1 prostate cancer xenografts without observed toxicity.
PK/PD data • Preclinical • Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression
12ms
Concurrent targeting AR/AR variants and AKR1C3 for advanced prostate cancer therapy (AUA 2023)
Resistant cell sublines generated from C4-2B cells resistant to enzalutamide (MDVR), apalutamide (ApalR), darolutamide (DaroR), or abiraterone (AbiR) were treated with LX-1 or their respective antiandrogen and cell number was determined. We generated novel small molecule inhibitors that concurrent target AR/AR-variant and AKR1C3. These compounds, specifically LX-1, effectively reduce CRPC growth and synergize with antiandrogens including enzalutamide in vitro and in vivo, suggesting potential for treating advanced prostate cancer.
Metastases
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AR splice variant 7 • AKR1C3 overexpression • AKR1C3 expression
|
enzalutamide capsule • abiraterone acetate • Nubeqa (darolutamide) • Erleada (apalutamide)
1year
Establishing a Proteomics-Based Signature of AKR1C3-Related Genes for Predicting the Prognosis of Prostate Cancer. (PubMed, Int J Mol Sci)
Furthermore, there was a close correlation between the sensitivity of PCa patients to bicalutamide and docetaxel and the expression levels of the eight risk genes. We found that PCa cells with a high expression of AKR1C3 have high proliferation ability and high migration ability and were insensitive to enzalutamide. AKR1C3-associated genes had a significant role in the process of PCa, immune responses, and drug sensitivity and offer the potential for a novel model for prognostic prediction in PCa.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3) • CDC20 (Cell Division Cycle 20) • ITK (IL2 Inducible T Cell Kinase) • POLR2L (RNA Polymerase II, I And III Subunit L) • SRSF3 (Serine And Arginine Rich Splicing Factor 3) • TIMM13 (Translocase Of Inner Mitochondrial Membrane 13)
|
AKR1C3 overexpression
|
docetaxel • enzalutamide capsule • bicalutamide
over1year
Development of highly potent and specific AKR1C3 inhibitors to restore the chemosensitivity of drug-resistant breast cancer. (PubMed, Eur J Med Chem)
Co-administration of these AKR1C3 inhibitors significantly reversed the doxorubicin (DOX) resistance in a resistant breast cancer cell line. Therefore, the novel AKR1C3 specific inhibitors developed in this work may serve as effective adjuvants to overcome DOX resistance in breast cancer treatment.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression
|
doxorubicin hydrochloride
almost2years
AKR1C3 expression in T acute lymphoblastic leukemia/lymphoma for clinical use as a biomarker. (PubMed, Sci Rep)
The AKR1C3 expression in peripheral blood by Protein Wes and RT-qPCR showed concordance in relapsed/refractory and/or minimal residual T-ALL cases. Sigma/Millipore Anti-AKR1C3 antibody and mouse monoclonal, clone NP6.G6.A6 can be used to aid in AKR1C expression of T-ALL and in cases of relapsed/refractory and/or minimal residual disease.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression • AKR1C3 expression
almost2years
Knockdown of AKR1C3 Promoted Sorafenib Sensitivity Through Inhibiting the Phosphorylation of AKT in Hepatocellular Carcinoma. (PubMed, Front Oncol)
AKR1C3 can induce sorafenib resistance through promoting the phosphorylation of AKT in HCC. AKR1C3 inhibitors may be used in conjunction with sorafenib to become a better therapeutic target for HCC.
Journal
|
AKT1 (V-akt murine thymoma viral oncogene homolog 1) • AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression
|
sorafenib
2years
Preclinical evaluation of TFX05-01, a selective AKR1C3- targeted prodrug for solid tumor (AACR 2022)
TFX05-01 is a novel selective AKR1C3-activated prodrug, which is different from traditional non-selective alkylating agents for cancer therapy. Preclinical studies have shown profound in vivo efficacy of TFX05-01 in AKR1C3 overexpressed mouse tumor xenograft models without marked toxicity. TFX05-01 represents a novel treatment option for AKR1C3 expressing solid cancers.
Preclinical
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression • AKR1C3 expression
over2years
Synthesis, antitumor activity and in silico analyses of amino acid derivatives of artepillin C, drupanin and baccharin from green propolis. (PubMed, Bioorg Med Chem)
All obtained derivatives were submitted to antiproliferative assays against four cancer cells (MCF-7, MDA MB-231, PC-3, and DU145) and two normal cell lines (MCF-10A and PNT-2) to evaluate their cytotoxicity. In general, the best activity was observed for compound6e, derived from drupanin, which exhibited half-maximal inhibitory concentration (IC) of 9.6 ± 3 μM and selectivity index (SI) of 5.5 against MCF-7 cells.In silicostudies demonstrated that these derivatives present coherent docking interactions and binding modes against AKR1C3, which might represent a possible mechanism of inhibition in MCF-7 cells.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression
over2years
A novel selective AKR1C3-activated prodrug AST-3424/OBI-3424 exhibits broad anti-tumor activity. (PubMed, Am J Cancer Res)
In the combination therapy, we showed that 3424 could enhance the efficacy of the standard care of chemotherapy in the CDX models. The results described here highlight that 3424 exhibits AKR1C3-dependent cytotoxicity in vitro and anti-tumor activity in vivo in a wide range of human cancer types, which support further development of 3424 as an anti-cancer agent for treating different types of cancers and the use of AKR1C3 as a biomarker to profile cancer patients and further guide patient selection for therapy with 3424.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression • AKR1C3 expression
|
OBI-3424
almost3years
Aldo-Keto Reductase 1C3 Mediates Chemotherapy Resistance in Esophageal Adenocarcinoma via ROS Detoxification. (PubMed, Cancers (Basel))
Here, we reported for the first time that AKR1C3 renders chemotherapy resistance through controlling ROS levels via AKT signaling in EAC cells. Targeting AKR1C3 may represent a novel strategy to sensitize EAC cells to conventional chemotherapy.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression • AKR1C3 expression
almost3years
AKR1C3 decreased CML sensitivity to Imatinib in bone marrow microenvironment via dysregulation of miR-379-5p. (PubMed, Cell Signal)
Altogether, our study identifies a novel signaling regulation of miR-379-5p/AKR1C3/EKR axis in regulating IM resistance in CML cell, and provides a scientific base for exploring AKR1C3 as a biomarker in impeding IM resistance in CML.
Journal
|
AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
|
AKR1C3 overexpression • AKR1C3 expression
|
imatinib