The ALDH1B1 Knockout TE1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human TE1 esophageal squamous cell carcinoma cell line. This product provides a loss-of-function model for ALDH1B1, generated through CRISPR/Cas9-mediated gene disruption. The polyclonal format ensures a heterogeneous population of edited cells, facilitating studies of gene function without clonal selection constraints. Researchers can utilize these cells to investigate ALDH1B1 in cancer biology, aldehyde detoxification, and retinoic acid metabolism.
The TE1 cell line is a human esophageal squamous cell carcinoma model widely used in oncology for studying pathogenesis, drug response, and carcinogenesis mechanisms. It retains squamous epithelial characteristics, including keratin expression and relevant signaling pathways. TE1 cells provide a consistent platform for tumor biology research, such as proliferation, invasion, and stemness. ALDH1B1 knockout in these cells enables dissection of gene functions in esophageal cancer.
ALDH1B1 encodes an aldehyde dehydrogenase that catalyzes oxidation of aldehydes, converting retinaldehyde to retinoic acid and detoxifying lipid peroxidation-derived aldehydes. Transcriptionally controlled by ??-catenin/TCF, retinoic acid receptors, and PPAR??, it functions downstream of NF-??B. ALDH1B1 interacts with ALDH1 family members, CYP450 enzymes, and alcohol dehydrogenase. It promotes retinoic acid synthesis, activating RAR/RXR receptors to regulate transcription. The enzyme also scavenges ROS by eliminating toxic aldehydes. Knockout impairs retinoic acid signaling and increases sensitivity to aldehyde cytotoxicity.
ALDH1B1 is implicated in esophageal cancer stem cell maintenance, chemoresistance, and metabolic adaptation to oxidative stress. This knockout model allows dissection of ALDH1B1’s role in these processes. Loss of ALDH1B1 reduces retinoic acid synthesis, altering differentiation and potentially increasing sensitivity to retinoid therapies. The model also enables study of endogenous aldehyde detoxification during lipid peroxidation, a tumor-associated stress. Scientists can investigate compensatory mechanisms by other ALDH isoforms and assess viability under oxidative conditions.
Applications include esophageal cancer stem cell research using ALDEFLUOR assays and flow cytometry for stem markers, and aldehyde metabolism studies via cell viability under aldehyde challenge. Validation can be performed by Western blot and RT-qPCR, while retinoic acid signaling reporter assays assess pathway activity. RNA-seq transcriptomics can profile expression changes upon ALDH1B1 disruption, and chemoresistance assays test drug sensitivity. This polyclonal knockout tool supports diverse investigations into ALDH1B1 in cancer and metabolism. For further details, contact Ascent Research.
