ACS5 Antibody

Introduction to ACS5 Antibody

The ACS5 antibody is a critical tool for detecting and studying acyl-CoA synthetase long-chain family member 5 (ACSL5), an enzyme central to lipid metabolism. ACSL5 activates long-chain fatty acids (C16–C20) by converting them into acyl-CoA derivatives, which are essential for lipid synthesis, storage, and β-oxidation . The ACS5 antibody enables researchers to investigate ACSL5’s expression, localization, and functional roles in metabolic and disease contexts, including cancer .

Research Findings in Metabolic Studies

ACSL5’s metabolic roles are context-dependent:

• Lipid Synthesis: In hepatocytes, ACSL5 overexpression increases triacylglycerol (TG) synthesis, while knockdown reduces TG accumulation and enhances β-oxidation .

• Tissue Specificity:

  • Liver: Directs fatty acids toward lipogenesis under normal conditions but promotes oxidation during metabolic stress .

  • Small Intestine: Localizes to lipid droplets and mitochondria, aiding dietary fat absorption .

  • Skeletal Muscle: Predominantly mitochondrial, suggesting a role in energy production .

These findings highlight ACSL5’s dual role in lipid metabolism, modulated by isoform expression and subcellular targeting .

Role in Cancer Research

ACSL5 overexpression is linked to tumor progression, particularly in colorectal cancer (CRC) and gliomas:

Colorectal Cancer

• Expression Patterns: ACSL5 levels are significantly elevated in CRC tissues compared to normal mucosa, correlating with poor tumor differentiation and invasiveness .

• Functional Impact:

  • Knockdown: Reduces proliferation, migration, and invasion in HT29 and SW480 cells while increasing apoptosis .

  • Overexpression: Enhances growth and metastasis in LOVO and SW620 cells via survivin upregulation and caspase-3/E-cadherin suppression .

Gliomas

• ACSL5 levels are markedly increased in glioblastoma multiforme (grade IV) compared to normal brain tissue. Palmitate-induced glioma cell growth is ACSL5-dependent, highlighting its role in fatty acid-driven oncogenesis .

Emerging Insights and Future Directions

Recent studies suggest ACSL5’s involvement in ferroptosis and peroxisome-related pathways , opening avenues for therapeutic targeting. For example:

• Ferroptosis: ACSL5 may modulate lipid peroxidation, a key ferroptosis mechanism .

• Therapeutic Potential: siRNA-mediated ACSL5 inhibition suppresses glioma growth in vivo , while CRC studies propose ACSL5 as a gene therapy target .

Key Challenges and Considerations

• Isoform Complexity: Human ACSL5 has three isoforms (739aa, 683aa, 659aa) with distinct subcellular localizations and functions . Antibodies must distinguish between these variants.

• Contradictory Roles: While ACSL5 promotes CRC and glioma progression, it acts as a tumor suppressor in urothelial cancers , underscoring tissue-specific mechanisms.