The ATF6 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the Ca Ski human cervical carcinoma line, featuring targeted disruption of the ATF6 gene. As a polyclonal pool, this product avoids clonal selection biases and provides a robust model for investigating ATF6 loss-of-function in epithelial cancer biology, with relevance to endoplasmic reticulum stress and the unfolded protein response (UPR).
Ca Ski cells are an HPV-16-positive human cervical epidermoid carcinoma line, originally isolated from a metastatic site. They are extensively used in cancer research for studying HPV-driven oncogenesis, cell migration, invasion, and drug responses. Retention of viral oncogenes E6 and E7 in these cells renders them particularly suitable for examining how viral proteins interface with host stress pathways, including the UPR.
ATF6 encodes an ER stress sensor and basic leucine zipper transcription factor. In unstressed cells, ATF6 is retained in the ER by BiP/GRP78. Upon stress, BiP dissociation triggers Golgi translocation, where sequential cleavage by S1P (MBTPS1) and S2P (MBTPS2) proteases releases the N-terminal fragment. This active form partners with NF-Y to drive transcription of UPR targets, including XBP1, ER chaperones such as BiP, GRP94, and calreticulin, ERAD machinery components, and the pro-apoptotic effector CHOP (DDIT3). ATF6 operates in concert with the IRE1?? and PERK arms of the UPR to balance adaptive repair and apoptosis.
In HPV-16-positive cervical cancer, ATF6-mediated UPR signaling may modulate tumor cell survival, apoptosis, and therapeutic sensitivity, potentially interacting with viral oncoprotein effects on ER homeostasis. The ATF6 knockout polyclonal cells enable dissection of ATF6??s contributions to ER stress resilience, migration, invasion, and viral replication in this malignancy. This model is valuable for exploring ER stress transducer targeting in cervical cancer and related HPV-associated diseases.
Typical experimental applications include Western blotting for ATF6 cleavage, RT-qPCR for UPR target genes, and luciferase reporter assays for ERSE activity. Functional assays can combine ER stress inducers (thapsigargin, tunicamycin) with apoptosis detection, migration/invasion tests, and drug sensitivity screening. Immunofluorescence allows monitoring of ATF6 localization, while pharmacological modulation probes ATF6-dependent phenotypes. For technical specifications and ordering, please contact Ascent Research.
