ALDH11A3 Antibody

Characteristics of the ALDH1A3 Antibody

The ALDH1A3 antibody (e.g., ab129815 from Abcam) is a rabbit polyclonal antibody designed for:

• Applications: Immunohistochemistry (IHC-P), immunoprecipitation (IP), Western blot (WB), and immunocytochemistry (ICC/IF).

• Reactivity: Human, mouse, and rat samples.

• Technical specifications:

  Parameter	Detail	Source
  Predicted band size	56 kDa
  Exposure time (IP)	20 minutes (ECL technique)
  Validation	Staining in PC3 cells (ICC/IF)

This antibody is widely cited (36+ publications) and validated for detecting ALDH1A3 in cancer models, including breast, lung, and brain metastases.

Detection in Cancer Subtypes

ALDH1A3 is overexpressed in aggressive cancers, such as triple-negative breast cancer (TNBC) and non-small cell lung cancer (NSCLC). The antibody enables:

• Immunohistochemical localization: ALDH1A3 is enriched at tumor-stromal boundaries in brain metastases (BM) and correlates with early metastatic phases .

• Western blot validation: Confirms ALDH1A3 downregulation in shRNA-treated cells (e.g., MDA-MB-231, MDA-MB-468) .

Functional Studies in Metastasis

ALDH1A3 promotes invasion and metastasis via mechanisms including:

• Protease regulation: Increases tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA), enhancing plasmin activity to degrade the extracellular matrix (ECM) .

• GABA metabolism: ALDH1A3-driven GABA production enhances metastatic potential, as shown in breast cancer models .

Modulation of CSC Markers

ALDH1A3 inversely regulates CD24 and CD44 expression, key CSC markers:

This shift reduces the CD24⁻CD44⁺ population (a mesenchymal CSC subset) and increases CD24⁺CD44⁺ cells, altering epithelial-to-mesenchymal transition (EMT) dynamics .

Metabolic Reprogramming

ALDH1A3 redirects glucose metabolism:

• ↓ Glycolysis: Reduces extracellular acidification rate (ECAR) and reactive oxygen species (ROS).

• ↑ Oxidative phosphorylation: Increases oxygen consumption rate (OCR) .

• Retinoic acid (ATRA) production: ALDH1A3 converts retinal to ATRA, driving gene expression changes linked to differentiation or proliferation .

Targeting ALDH1A3 in Brain Metastases

In TNBC brain metastasis (BCBM) models:

• ALDH1A3 knockdown reduces adhesion, migration, and BM initiation .

• Glycolysis inhibition (2-deoxy-D-glucose, 2DG) synergizes with ALDH1A3 suppression to limit tumor growth .

ALDH1A3 Inhibitors

General ALDH inhibitors (e.g., disulfiram) and isoform-specific blockers are under investigation. ALDH1A3’s role in NFY/KAT2B-mediated chromatin remodeling (e.g., in pulmonary arterial hypertension) highlights its broader therapeutic potential .