The ANXA10 Knockout HeLa Polyclonal Cells product delivers a CRISPR/Cas9-mediated polyclonal knockout population targeting the ANXA10 locus in the HeLa cervical carcinoma cell line. This cell pool is engineered through introduction of guide RNAs and Cas9 nuclease, generating a heterogeneous population of cells with targeted gene disruption. Unlike clonal knockout lines, the polyclonal format preserves genetic variability, more closely reflecting the heterogeneity of tumor cell populations. The product is supplied as a cryopreserved stock immediately after editing, allowing researchers to recover and expand cultures for downstream applications. This population-based model is especially valuable for preliminary functional screening, drug sensitivity profiling, and studies that avoid clonal selection bias.
The HeLa host cell line is an HPV18-positive human cervical adenocarcinoma epithelial line used extensively as an immortalized cancer model. Its rapid growth, ease of transfection, and well-documented molecular profile make it ideal for gene-editing studies. HPV18 oncoproteins E6 and E7 inactivate p53 and pRb, respectively, disrupting cell cycle control and apoptosis. This background provides a consistent platform for evaluating ANXA10 tumor suppressor functions.
ANXA10 encodes a member of the annexin family of calcium-dependent phospholipid-binding proteins, which are involved in membrane trafficking, endocytosis, exocytosis, and signal transduction. This protein is implicated as a tumor suppressor in multiple cancer types, with its expression frequently downregulated through promoter CpG methylation by DNA methyltransferases, a process regulated in part by the transcription factor SP1. Mechanistically, ANXA10 interacts with calcium ions, membrane phospholipids, and S100 family proteins, and its loss leads to derepression of the MAPK/ERK pathway. Specifically, signaling through RAS, RAF, MEK, and ERK is enhanced, culminating in increased expression of cyclin D1 and a shift in the Bcl-2:Bax ratio that inhibits caspase-3 activation and apoptosis. Thus, ANXA10 normally functions to restrain proliferative signaling and promote apoptotic sensitivity.
In HeLa cells, ANXA10 knockout mirrors the epigenetic silencing found in gastric, hepatocellular, colorectal, and breast cancers. Combined with HPV-driven oncogenic stress, the loss of ANXA10 may amplify MAPK/ERK signaling and survival pathways, offering a model to study synergistic effects in cervical carcinogenesis and drug resistance.
This polyclonal ANXA10 knockout cell population enables research into cancer biology, tumor suppression, drug resistance, and MAPK/ERK-dependent apoptosis. Typical assays include western blotting and RT-qPCR for targets like cyclin D1 and caspase-3, Annexin V staining, MTT proliferation, and invasion assays. Comparison with wild-type HeLa defines ANXA10’s roles. Contact Ascent Research for details.
