In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The ALKBH5 Knockout A549 Cell Line is a CRISPR/Cas9-edited human lung adenocarcinoma cell line with targeted disruption of the RNA demethylase ALKBH5. This loss-of-function model increases m6A modification on target mRNAs including FOXM1 and NANOG, enabling studies of epitranscriptomic regulation in cancer. Designed for applications such as MeRIP-seq, RNA stability assays, and phenotypic analyses of proliferation and invasion, this cell line is ideal for investigating hypoxia-mediated RNA processing and m6A-dependent gene expression in lung adenocarcinoma.
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Rabbit Synovial Fibroblast Medium
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The ALKBH5 Knockout A549 Cell Line is a CRISPR/Cas9-edited knockout derivative of the A549 human lung adenocarcinoma epithelial cell line, providing a stable loss-of-function model for the RNA demethylase ALKBH5, which removes N6-methyladenosine (m6A) from mRNA. This targeted gene disruption enables researchers to dissect ALKBH5??s roles in mRNA processing, stability, and translation within a lung cancer context. The line is suitable for a wide array of molecular and cellular assays, offering a renewable resource for studying m6A modification dynamics and cancer biology.
The parental A549 line, originally established from a 58-year-old male with lung adenocarcinoma, serves as a widely recognized model of type II alveolar epithelial cells and lung adenocarcinoma. These cells exhibit hallmark characteristics of lung cancer biology, including dysregulated proliferation, invasive potential, and hypoxia-inducible responses. Extensively employed in oncology research, A549 cells are amenable to CRISPR-based genetic engineering, positioning the ALKBH5 knockout derivative as a relevant system for investigating the interplay between RNA modifications and lung cancer mechanisms.
ALKBH5 is an m6A eraser that demethylates N6-methyladenosine in mRNA, influencing splicing, stability, and translation via m6A readers such as YTHDF1/2/3 and YTHDC1/2. Its expression is induced by HIF-1?? under hypoxia and modulated by TGF-?? signaling. Knockout increases m6A on targets like FOXM1 and NANOG, altering cell proliferation and epithelial-mesenchymal transition programs. ALKBH5 functions alongside the methyltransferase complex METTL3-METTL14-WTAP and the eraser FTO, and interacts with nuclear speckles and splicing factors, integrating RNA modification with gene expression regulation.
In the A549 lung adenocarcinoma background, ALKBH5 knockout elevates m6A levels on transcripts such as FOXM1 and NANOG, providing a system to probe RNA modification-dependent mechanisms. This model is particularly valuable for studying hypoxia-driven gene regulation via HIF-1?? and for assessing impacts on proliferation, invasion, and epithelial-mesenchymal transition. By comparing with wild-type controls, researchers can delineate ALKBH5-specific contributions to cancer phenotypes and the broader m6A epitranscriptome.
The ALKBH5 Knockout A549 Cell Line enables a range of experimental approaches, including global m6A profiling via MeRIP-seq, m6A dot blot, RT-qPCR and western blot analysis of target genes, and RNA stability measurements. Functional assays such as cell proliferation and invasion studies allow phenotypic assessment of ALKBH5 loss. This model is well-suited for investigating hypoxia-mediated RNA regulation, screening for context-dependent phenotypes, and exploring the role of m6A dynamics in lung adenocarcinoma progression. For further details or to discuss specific research needs, please contact Ascent Research.
