ALDH3A2 Knockout Cell Lines

Gene: ALDH3A2

Official Full Name: aldehyde dehydrogenase 3 family member A2provided by HGNC

Gene Summary: Aldehyde dehydrogenase isozymes are thought to play a major role in the detoxification of aldehydes generated by alcohol metabolism and lipid peroxidation. This gene product catalyzes the oxidation of long-chain aliphatic aldehydes to fatty acid. Mutations in the gene cause Sjogren-Larsson syndrome. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

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Products Background Case study

Products

Catalog Number	Product Name	Species	Gene	Passage ratio	Mycoplasma testing	Price
KO00013	ALDH3A2 Knockout cell line （THP-1）	Human	ALDH3A2	1：2-1：4	Negative	Online Inquiry
KO39029	ALDH3A2 Knockout cell line (HeLa)	Human	ALDH3A2	1:3~1:6	Negative	Online Inquiry
KO39030	ALDH3A2 Knockout cell line (HCT 116)	Human	ALDH3A2	1:2~1:4	Negative	Online Inquiry
KO39031	ALDH3A2 Knockout cell line (HEK293)	Human	ALDH3A2	1:3~1:6	Negative	Online Inquiry
KO39032	ALDH3A2 Knockout cell line (A549)	Human	ALDH3A2	1:3~1:4	Negative	Online Inquiry

Background

ALDH3A2 Gene Knockout Cell Lines are precisely engineered cellular models created to disrupt the expression of the ALDH3A2 gene, which encodes for the enzyme aldehyde dehydrogenase 3A2. This gene plays a crucial role in the metabolism of various aldehydes and contributes to the cellular defense against oxidative stress. By knocking out this gene, researchers can investigate the physiological and pathological roles that aldehyde metabolism plays in cellular health, disease progression, and therapeutic responses.

The key function of these knockout cell lines lies in their ability to mimic conditions in which the ALDH3A2 enzyme is dysfunctional or absent, thus providing insights into its contributions to conditions such as fatty liver disease, neurodegeneration, and certain types of cancer. Mechanistically, the loss of ALDH3A2 activity leads to the accumulation of toxic aldehyde species, presenting a unique framework to study how cellular response pathways adapt to stress and injury.

The scientific importance of the ALDH3A2 Gene Knockout Cell Lines cannot be overstated, as they serve as vital tools in both basic and applied research settings. In translational research, these models offer a platform for drug discovery, toxicity screening, and the understanding of metabolic disorders. Their practical applications extend to the development of targeted therapies that could mitigate the effects of aldehyde toxicity.

What sets ALDH3A2 Gene Knockout Cell Lines apart from conventional cell lines is their specificity and reliability in modeling ALDH3A2-related processes, thereby providing researchers with a powerful tool to elucidate molecular mechanisms underpinning various diseases. Furthermore, their robust performance enhances reproducibility in experimental outcomes, essential for advancing scientific knowledge.

Researchers and clinicians seeking to broaden their understanding of metabolic regulation and oxidative stress will find value in these knockout cell lines, as they open avenues for innovative research and potential clinical applications. Our company is committed to providing high-quality, validated biological products, and our expertise in genetic engineering ensures that ALDH3A2 Gene Knockout Cell Lines meet the rigorous standards necessary for impactful scientific inquiry.

Case study

ALDH3A2 Gene Knockout Cell Lines for Gastric Adenocarcinoma Research

Research Focus

Investigate the role of ALDH3A2 (Aldehyde Dehydrogenase 3 Family Member A2) in gastric adenocarcinoma (STAD) progression and its potential as a prognostic biomarker and immunotherapy target using CRISPR/Cas9-generated ALDH3A2 knockout (KO) cell lines.

Background

1. Gastric Adenocarcinoma and Biomarker Needs

Gastric adenocarcinoma is a common digestive system malignancy with high mortality, affecting ~990,000 individuals annually. Despite advances in treatment, the 5-year survival rate remains below 20% worldwide, underscoring the need for novel biomarkers for early diagnosis and prognosis .

2. ALDH3A2 in Metabolism and Cancer

ALDH3A2 is an enzyme involved in aldehyde detoxification and lipid peroxidation, but its role in gastric cancer is unclear. Previous studies suggest ALDH3A2 mutations are linked to Sjogren-Larsson syndrome, but its function in tumorigenesis remains unexplored .

3. Immune Checkpoints and Cancer Therapy

Immune checkpoint proteins (e.g., PD-1, PD-L2, CTLA-4) play a key role in tumor immune evasion. Identifying genes that modulate these checkpoints could reveal new therapeutic strategies for gastric cancer .

Solution

1. Generation of ALDH3A2 KO Cell Lines

Method: CRISPR/Cas9 genome editing was used to disrupt ALDH3A2 in human gastric cancer cell lines (HGC-27, MGC-803). KO was confirmed by qPCR and Western blotting, showing complete loss of ALDH3A2 mRNA and protein expression .

Validation: ALDH3A2 KO cells exhibited altered metabolic profiles and enhanced sensitivity to immune checkpoint inhibitors compared to wild-type cells.

2. Functional Assays in ALDH3A2 KO Cells

Prognostic Significance: ALDH3A2 KO cells showed reduced survival in vitro and were associated with poor clinical outcomes in patient samples. Kaplan-Meier analysis revealed patients with low ALDH3A2 expression had shorter overall survival (OS) than those with high expression (

P<0.05

) .

Metabolic Pathway Analysis: Gene Set Enrichment Analysis (GSEA) showed ALDH3A2 KO cells had disrupted fatty acid metabolism and β-alanine metabolism, pathways linked to tumor progression .

Immune Checkpoint Regulation: ALDH3A2 KO cells upregulated PDCD1 (PD-1), PDCD1LG2 (PD-L2), and CTLA-4 at both mRNA and protein levels, suggesting a role in immune evasion .

3. Clinical and Immunological Correlations

Tumor Grade Association: ALDH3A2 expression was higher in low-grade (I/II) vs. high-grade (III/IV) gastric tumors, indicating a potential role in tumor differentiation .

Immune Cell Infiltration: ALDH3A2 KO cells showed reduced M1 macrophage infiltration, a key component of the antitumor immune response, while promoting immune suppressive microenvironments .

Therapeutic Potential: Knockdown of ALDH3A2 sensitized cells to anti-PD-1 therapy, suggesting ALDH3A2 inhibitors could enhance immunotherapy efficacy .

Conclusion

1. Mechanistic Insights

ALDH3A2 regulates gastric cancer progression through two key mechanisms:

Metabolic Regulation: ALDH3A2 maintains lipid and amino acid metabolism, and its loss disrupts energy homeostasis, promoting tumor aggression .

Immune Checkpoint Control: ALDH3A2 suppresses PD-1, PD-L2, and CTLA-4 expression, preserving antitumor immune responses. KO cells lose this suppression

Please note that all services are for research use only. Not intended for any clinical use.

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