The BTK Knockout Ca Ski Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human cervical carcinoma cell line Ca Ski. This population consists of a heterogeneous mixture of cells carrying Cas9-induced disruptions in the BTK gene, enabling loss-of-function studies of Bruton’s tyrosine kinase (BTK) at a population level. The polyclonal format avoids the selection biases inherent in clonal isolation and is well-suited for examining BTK??s role in an epithelial cancer background.
Ca Ski is an adherent epithelial cell line originally established from a cervical epidermoid carcinoma metastasis and is characterized by the presence of an integrated human papillomavirus type 16 (HPV-16) genome. It is widely used as a model system for HPV-driven cervical carcinogenesis, displaying deregulated proliferation and survival signaling. This line provides a distinct, non-hematopoietic environment to study BTK, which is predominantly investigated in B-cell lineages, thereby facilitating exploration of its broader functions in virus-associated epithelial tumors.
BTK is a non-receptor tyrosine kinase critical for B-cell receptor (BCR) signaling. Upon BCR activation, upstream kinases LYN and SYK phosphorylate BTK, enabling interaction with BLNK and phosphorylation of PLCG2. This generates IP3 and DAG, which promote calcium flux and PKC-mediated activation of NF-??B and NFAT. BTK also propagates signals via PI3K-AKT and MAPK/ERK cascades and associates with adaptors GAB1 and PIP5K. Additionally, it functions in Fc epsilon RI and cytokine receptor pathways (IL-5, IL-6), linking extracellular stimuli to transcriptional programs of proliferation and differentiation.
In cervical cancer, BTK??s role is under exploration. While classically a B-cell kinase, BTK expression and function have been noted in certain epithelial tumors, potentially influencing cell survival and migration. The Ca Ski line, with integrated HPV-16, is ideal for studying BTK in virus-driven oncogenesis. This polyclonal knockout model permits assessment of BTK-dependent phenotypes without clonal selection artifacts, aiding dissection of signaling pathways that may be distinct from canonical B-cell functions.
These polyclonal knockout cells enable diverse experimental approaches. Western blotting can confirm BTK loss and reduced phosphorylation of PLCG2, AKT, and ERK. Proliferation (MTT) and apoptosis (Annexin V) assays quantify growth and survival phenotypes. Phospho-signaling analysis reveals alterations in LYN, SYK, and NF-??B networks. Migration assays assess BTK??s role in cell motility. The model also supports pharmacological studies targeting BTK or related pathways, particularly in the context of HPV-positive cervical cancer. For product inquiries, please contact Ascent Research.
