The HNRNPA2B1 Knockout HeLa Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal HeLa population with targeted disruption of the HNRNPA2B1 gene. This loss-of-function model maintains population heterogeneity while abolishing HNRNPA2B1 protein, offering a versatile tool for studying gene-dependent processes in a diverse cellular context without single-cell cloning artifacts.
The parental HeLa cell line is a cervical adenocarcinoma model with epithelial morphology, HPV18 positivity, and inactivation of p53 and Rb by viral oncoproteins E6 and E7. This renders cells highly proliferative and transformed, making HeLa a classic platform for cancer and viral carcinogenesis studies. The HNRNPA2B1 knockout in this background permits dissection of gene function under conditions of deregulated cell cycle and apoptosis control.
HNRNPA2B1 encodes an RNA-binding protein that regulates alternative splicing, mRNA transport, and translation. It interacts with splicing factors SRSF1, U2AF2, HNRNPA1, and HNRNPC, and mRNA export factors ALYREF and NXF1. Upstream transcription factors MYC, NF-??B (RELA), STAT3, and SP1 drive its expression. HNRNPA2B1 modulates key cancer targets: promoting PKM isoform switching, stabilizing AR-V7 mRNA, enhancing MYC and CCND1 expression, and regulating Bcl-xL splicing to inhibit apoptosis. These functions link it to PI3K-AKT (PIK3CA, AKT1), STAT3 (JAK2, STAT3), and NF-??B (RELA, IKBKB) pathways.
In HeLa cells where p53 and Rb are inactivated, HNRNPA2B1 knockout disrupts splicing and reduces pro-proliferative and anti-apoptotic factors, impairing growth and metastasis. This polyclonal model enables study of HNRNPA2B1-driven RNA processing in cervical adenocarcinoma and other cancers like glioblastoma, breast, and lung. It also facilitates investigation of telomere maintenance and DNA damage response in HPV-associated cancers, with the polyclonal population reflecting tumor heterogeneity.
These cells are ideal for RNA processing studies via RNA-seq, RIP, and co-immunoprecipitation. Functional assays such as proliferation, migration, and apoptosis assays reveal HNRNPA2B1-dependent phenotypes, while western blotting and RT-qPCR validate downstream targets including MYC and CCND1. The model supports drug target validation and pathway analysis in NF-??B, STAT3, and PI3K-AKT signaling contexts. For further information or to discuss custom applications, please contact Ascent Research.
