In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The METTL3 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited human bronchial epithelial cell line lacking functional METTL3, the catalytic subunit of the m6A methyltransferase complex. This non-tumorigenic BEAS-2B-derived model enables dissection of epitranscriptomic regulation in lung biology. METTL3, along with METTL14 and WTAP, catalyzes m6A modification on mRNAs encoding critical factors such as MYC, EGFR, and SOX2, with reader proteins YTHDF1?C3 mediating downstream effects on RNA stability and translation. Applications include RNA modification studies, lung cancer research, and drug screening.
CHID1 Knockout HT29 Polyclonal Cells
Cat. No. ARG14004
ANXA3 Knockout HEK293T Polyclonal Cells
Cat. No. ARG25691
IGFBP5 Knockout NCI-H1703 Polyclonal Cells
Cat. No. ARG36560
DOCK4 Knockout HAP1 Polyclonal Cells
Cat. No. ARG39584
CRABP2 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7077
FYTTD1 Knockout 786-O Polyclonal Cells
Cat. No. ARG5353
The METTL3 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited human cell line engineered to disrupt the METTL3 gene, resulting in a loss-of-function model for studying N6-methyladenosine (m6A) RNA modification. This gene-edited cell line provides a stable and renewable resource for investigating the biological functions of METTL3 in a bronchial epithelial context.
The parental BEAS-2B cell line is an immortalized, non-tumorigenic human bronchial epithelial cell line derived from normal bronchial epithelium and transformed with SV40 large T-antigen. BEAS-2B cells retain many characteristics of primary bronchial epithelial cells, including the ability to undergo squamous differentiation and respond to environmental stimuli, making them a widely used model for respiratory biology and lung carcinogenesis studies.
METTL3 encodes the catalytic subunit of the METTL3/METTL14/WTAP N6-adenosine-methyltransferase complex, which deposits m6A modifications on mRNA transcripts. This modification is recognized by YTHDF1, YTHDF2, and YTHDF3 reader proteins that influence mRNA stability, translation efficiency, splicing, and decay. METTL3 activity is regulated by upstream factors such as the transcription factor MYC, the tumor suppressor TP53, and various cellular stress signals. Key downstream targets include mRNAs encoding MYC, EGFR, and SOX2, creating feedback and feedforward loops that modulate cell proliferation, stemness, and oncogenic signaling.
In the BEAS-2B cellular context, METTL3 knockout eliminates the deposition of m6A on target transcripts, disrupting the coordinated regulation of gene expression networks critical for epithelial homeostasis and response to oncogenic cues. Given the involvement of METTL3 in lung cancer progression and the sensitivity of bronchial epithelial cells to carcinogens, this knockout cell line serves as a powerful tool for dissecting how m6A modification influences malignant transformation, inflammatory responses, and differentiation in the airway epithelium.
Research applications of the METTL3 Knockout BEAS-2B Cell Line include epitranscriptomic profiling, RNA modification studies, lung cancer biology, and drug discovery screens. Researchers can employ m6A quantification methods such as dot blot or LC-MS/MS alongside western blotting to confirm METTL3 loss. Functional assays may involve RT-qPCR to measure target gene expression, RNA stability and immunoprecipitation with anti-m6A antibodies to assess methylation status, as well as cell proliferation and migration assays to evaluate phenotypic consequences. For further information, please contact Ascent Research.
