The IGF2BP2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, designed for targeted disruption of the IGF2BP2 gene. This product provides a heterogeneous pool of gene-edited cells, enabling robust loss-of-function studies without the biases associated with single-cell cloning. The polyclonal format preserves genetic background variability while achieving efficient target-gene disruption, making it ideal for population-level functional analyses.
The HeLa host cell line is an immortalized human epithelial cell line derived from a cervical adenocarcinoma biopsy of Henrietta Lacks. These cells are HPV18-positive and widely employed as a model system for human epithelial biology, cancer research, and signaling pathway analysis. HeLa cells retain key oncogenic properties and are highly amenable to genetic manipulation, making them a classic platform for investigating tumor cell proliferation, migration, and metabolic regulation.
IGF2BP2 encodes an insulin-like growth factor 2 mRNA-binding protein that functions as an m6A reader, binding N6-methyladenosine modifications on target mRNAs to stabilize them and enhance their translation. Upstream, IGF2BP2 is regulated by factors such as MYC, HIF1A, and the m6A methyltransferase complex including METTL3 and METTL14, while its activity can be modulated by demethylases like FTO and ALKBH5. IGF2BP2 directly binds and stabilizes mRNAs of oncogenes and cell cycle regulators, including MYC, CDK6, and GLUT1, as well as IGF2 and ACTB transcripts, thereby driving proliferation and metabolic reprogramming. It interacts with other RNA-binding proteins such as HNRNPA2B1, ELAVL1, and YTHDF1, as well as with METTL3, integrating m6A modification with post-transcriptional control. These interactions position IGF2BP2 at the nexus of RNA regulation and cancer cell growth, particularly through the PI3K-AKT-mTOR pathway, where it promotes translation of key effectors.
In the HeLa cervical cancer model, disruption of IGF2BP2 provides a powerful tool to dissect m6A-dependent gene regulation in a well-characterized epithelial tumor context. Loss of IGF2BP2 is expected to reduce the stability and translation of its target mRNAs, attenuating oncogenic signaling downstream of MYC and PI3K-AKT-mTOR. This knockout model enables investigation of how dynamic m6A reading influences cell cycle progression, glycolytic metabolism via GLUT1, and insulin/IGF signaling. Moreover, it permits examination of the functional interplay between m6A readers, writers, and erasers in a cancer-relevant background, shedding light on epigenetic and post-transcriptional mechanisms driving cervical adenocarcinoma.
These polyclonal knockout cells are suitable for a wide range of functional assays, including Western blotting and RT-qPCR to verify target knockdown and downstream effects, as well as RNA-seq and MeRIP-seq to map transcriptome-wide m6A and expression changes. PAR-CLIP can be employed to directly interrogate IGF2BP2?CRNA interactions in comparative settings. Cell-based assays such as MTT/CCK8 proliferation analysis, Transwell migration assays, apoptosis detection, and flow cytometry-based cell cycle profiling allow detailed phenotypic characterization. The product serves as a valuable resource for cancer cell proliferation studies, m6A modification research, insulin signaling pathway dissection, and drug target validation for metabolic diseases and cancer. For further information and custom inquiries, please contact Ascent Research.
