The Importance of AKR1C2 as a Drug Target or Biomarker (G1646)

Target Name: AKR1C2

NCBI ID: G1646

AKR1C2

The Importance of AKR1C2 as a Drug Target or Biomarker

Introduction:
In the realm of drug discovery and development, identifying suitable drug targets or biomarkers plays a crucial role. One such target of interest is the enzyme AKR1C2, which has garnered attention due to its involvement in various diseases and its potential as a therapeutic target. This article explores the significance of AKR1C2 as a drug target or biomarker.

Understanding AKR1C2:
AKR1C2, short for Aldo-Keto Reductase Family 1 Member C2, is an enzyme that belongs to the aldo-keto reductase (AKR) superfamily. It is primarily expressed in the liver, breast, and prostate tissues, playing a multifaceted role in various physiological processes. The enzyme is involved in the metabolism of numerous endogenous compounds, such as steroid hormones, eicosanoids, and prostaglandins.

AKR1C2 as a Drug Target:
Research has demonstrated that AKR1C2 dysregulation is implicated in several diseases, making it an enticing target for therapeutic intervention. In certain cancers, such as breast, prostate, and ovarian cancer, AKR1C2 overexpression has been observed. This overexpression contributes to enhanced tumor cell proliferation, survival, and resistance to chemotherapy.

Targeting AKR1C2 using specific inhibitors has shown promising results. For example, inhibiting AKR1C2 has been found to reduce tumor growth in preclinical models of prostate and breast cancer. This highlights the therapeutic potential of AKR1C2 inhibitors in the treatment of these malignancies.

Moreover, AKR1C2 also plays a role in drug resistance. In prostate cancer, AKR1C2 has been implicated in the metabolism of anticancer agents, such as docetaxel and enzalutamide, leading to drug resistance. Inhibiting AKR1C2 can potentially improve the efficacy of these drugs and overcome resistance mechanisms, offering new opportunities for better patient outcomes.

AKR1C2 as a Biomarker:
Apart from being a drug target, AKR1C2 also holds promise as a biomarker for various diseases. The expression levels of AKR1C2 have been found to correlate with disease progression and prognosis in several cancers. In prostate cancer, higher AKR1C2 expression is associated with more aggressive disease and worse survival outcomes. Monitoring AKR1C2 expression could aid in patient stratification and predicting disease outcomes, allowing for personalized treatment approaches.

Additionally, AKR1C2 has been implicated in disorders such as polycystic ovary syndrome (PCOS) and endometriosis. In these conditions, altered expression of AKR1C2 has been identified. Utilizing AKR1C2 as a biomarker in the diagnosis or management of these diseases could potentially improve patient care and treatment strategies.

Future Perspectives and Conclusion:
The significance of AKR1C2 as a drug target and biomarker continues to gain recognition within the scientific community. Ongoing research aims to further elucidate its role in disease pathogenesis and validate its potential as a therapeutic target. Developing AKR1C2 inhibitors with increased potency and specificity remains an active area of investigation.

Additionally, efforts are being made to explore AKR1C2 as a diagnostic and prognostic biomarker. Identifying reliable biomarkers can aid in early disease detection, enabling timely intervention and improved patient outcomes. Furthermore, utilizing AKR1C2 as a biomarker could facilitate the development of companion diagnostics, allowing for targeted treatments based on individual patient characteristics.

In conclusion, AKR1C2 represents a promising drug target and biomarker due to its involvement in various diseases and physiological processes. Targeting AKR1C2 with specific inhibitors shows potential as a therapeutic strategy, while assessing AKR1C2 expression levels holds promise for disease prognosis and personalized treatment approaches. Continued research and development in this field may lead to the discovery of novel therapeutics and improved patient care.

Protein Name: Aldo-keto Reductase Family 1 Member C2

Functions: 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). Works in concert with the 5-alpha/5-beta-steroid reductases to convert steroid hormones into the 3-alpha/5-alpha and 3-alpha/5-beta-tetrahydrosteroids. Catalyzes the inactivation of the most potent androgen 5-alpha-dihydrotestosterone (5-alpha-DHT) to 5-alpha-androstane-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:15929998, PubMed:17034817, PubMed:17442338, PubMed:8573067). Also specifically able to produce 17beta-hydroxy-5alpha-androstan-3-one/5alphaDHT (PubMed:10998348). May also reduce conjugated steroids such as 5alpha-dihydrotestosterone sulfate (PubMed:19218247). Displays affinity for bile acids (PubMed:8486699)

The "AKR1C2 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about AKR1C2 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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