The ABCF2 Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ABCF2 gene in the human HeLa cell line. This loss-of-function model enables investigation of ABCF2-dependent processes without relying on single-cell cloning, thereby preserving natural cellular heterogeneity. The polyclonal format is suitable for pooled screening approaches and studies requiring a representative knockout background. CRISPR/Cas9-mediated gene disruption ensures stable ablation of ABCF2 function, providing a reliable tool for functional genomics and translational research.
The HeLa cell line, derived from cervical adenocarcinoma, is an HPV18-positive, aneuploid, adherent epithelial line extensively used in cancer biology and drug screening. Its well-characterized pathways include mTOR signaling and the translational machinery, making it suitable for studying ABCF2??s role in protein synthesis and drug resistance. The cervical cancer origin renders these cells pertinent to gynecologic malignancy research.
ABCF2 encodes an atypical ATP-binding cassette transporter involved in translation initiation and ribosome biogenesis. It functions as a translation factor, interacting with ribosomal subunits and initiation factors eIF2 and eIF3 to facilitate ribosome assembly. ABCF2 expression is positively regulated by NRF2 transcription factor and mTOR kinase, placing it within the mTOR-S6K1-eIF4E signaling axis. By modulating translation of anti-apoptotic mRNAs such as BCL2 and MCL1, ABCF2 supports cell survival. Knockout of ABCF2 is expected to impair mTOR-driven protein synthesis and survival signaling, altering chemotherapeutic responses.
In the HeLa background, loss of ABCF2 disrupts the translational machinery that sustains oncogenic traits. Given HeLa cells?? utility as a cervical cancer model, ABCF2 knockout directly impacts studies on drug resistance??a key challenge in treating cervical, ovarian, and breast cancers. By impairing the synthesis of pro-survival factors, the knockout sensitizes cells to apoptosis induced by cisplatin and paclitaxel, agents commonly used in clinical protocols. This polyclonal population maintains the heterogeneous nature of tumor cell populations, offering a more clinically relevant tool than monoclonal derivatives. Researchers can dissect how ABCF2-dependent translation influences cancer cell fitness and drug tolerance under physiologically relevant conditions.
This product enables a broad spectrum of experimental approaches. Researchers can employ polysome profiling to assess ribosome occupancy changes and combine it with ribosome footprinting to map translationally regulated transcripts. Western blotting with antibodies targeting eIF2, eIF4E, or ribosomal proteins quantifies pathway alterations, while RT-qPCR monitors transcriptional changes. Drug sensitivity assays using cisplatin or paclitaxel, along with apoptosis and proliferation assays, quantify functional consequences of ABCF2 loss. RNA-sequencing reveals transcriptome-wide shifts, aiding identification of translationally controlled targets. These polyclonal cells are suitable for CRISPR screening library comparisons and functional validation of hits from genomic studies. For additional product information or technical support, please contact Ascent Research.
