The ALDH1A1 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function analyses of the ALDH1A1 gene. This product consists of a heterogeneous pool of Ca Ski cells carrying targeted gene disruptions introduced by CRISPR/Cas9-mediated editing, without single-cell cloning. The polyclonal format preserves genetic diversity, minimizing clonal artifacts and enabling robust examination of ALDH1A1 function across a population. This knockout tool is well-suited for both pooled and high-throughput experimental configurations in cervical cancer research.
The Ca Ski host cell line is a human cervical epidermoid carcinoma epithelial line derived from a metastatic site. Ca Ski cells are positive for human papillomavirus type 16 (HPV-16) and display aggressive tumorigenic behavior, establishing them as a widely used model for metastatic cervical carcinoma. This cell line recapitulates hallmarks of cervical cancer progression, including deregulated proliferation and invasive capacity, and is therefore valuable for investigating molecular mechanisms of metastasis and therapeutic resistance. The presence of the HPV-16 genome further allows studies of viral oncoprotein crosstalk with host regulatory networks.
ALDH1A1 encodes a cytosolic aldehyde dehydrogenase that irreversibly converts retinaldehyde to retinoic acid in an NAD+-dependent manner, a key step in retinoid metabolism. Retinoic acid subsequently activates RAR?? and RXR nuclear receptors to drive transcription of target genes such as HOX clusters and CYP26A1, while also modulating stemness regulators including OCT4 and SOX2. ALDH1A1 activity is regulated by upstream signals from the WNT/??-catenin and NOTCH pathways and the transcription factor FOXM1. The enzyme additionally participates in detoxification of aldehydes, supporting cellular resistance to oxidative stress. In the canonical retinoid cascade, retinaldehyde is generated by RDH enzymes, and upon ALDH1A1-mediated oxidation, all-trans retinoic acid is shuttled by CRABP1 to nuclear receptors, culminating in transcriptional reprogramming.
In Ca Ski cervical cancer cells, ALDH1A1 is linked to cancer stem cell (CSC) properties, including enhanced spheroid formation, self-renewal, and chemoresistance. Retinoic acid signaling through ALDH1A1 influences differentiation and stemness, contributing to tumor heterogeneity and relapse. Moreover, ALDH1A1-mediated aldehyde detoxification may protect cells from metabolic stress and chemotherapeutic agents, reinforcing tumorigenicity. Consequently, ablating ALDH1A1 in this polyclonal knockout population provides a physiologically relevant system to dissect CSC biology and resistance mechanisms specific to HPV-16-positive cervical carcinoma.
Researchers can employ this knockout model to explore ALDH1A1??s roles in cancer stem cell maintenance, retinoic acid signaling, and drug sensitivity. Representative assays include ALDEFLUOR activity measurement, Western blotting for ALDH1A1 protein, RT-qPCR for stemness markers, spheroid formation assays, MTT-based viability tests, and retinoic acid quantification by LC-MS. The polyclonal format is compatible with pooled functional genomics and high-content screening applications. For further product details or technical support, please contact Ascent Research.
