ALDH1B1 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast cancer cell line, engineered for loss-of-function studies of the ALDH1B1 gene. This product provides a heterogeneous pool of cells with disrupted ALDH1B1 expression, enabling robust investigation of gene function without clonal selection effects. The polyclonal format retains the genetic diversity essential for capturing population-level responses in cancer biology and drug sensitivity assays.
The parental T-47D cell line is an epithelial breast carcinoma model originally isolated from a pleural effusion of a metastatic ductal carcinoma. These cells are estrogen receptor-positive, progesterone receptor-positive, and androgen receptor-positive, making them a well-established in vitro system for hormone-responsive breast cancer research. T-47D cells exhibit hormone-dependent growth and retain characteristic features of luminal breast cancer, including sensitivity to endocrine therapies and expression of epithelial markers.
ALDH1B1 encodes a mitochondrial aldehyde dehydrogenase that oxidizes acetaldehyde and retinaldehyde, contributing to ethanol metabolism and retinoic acid biosynthesis. The enzyme is regulated by NFE2L2 (Nrf2) in response to oxidative stress and is further modulated by Wnt/??-catenin signaling. ALDH1B1 converts retinaldehyde into retinoic acid, which activates RAR??/RXR transcription factors to control differentiation and stemness genes. It also detoxifies reactive aldehydes such as acetaldehyde, reducing oxidative damage. Downstream, ALDH1B1 activity promotes retinoic acid production and ROS mitigation, while interacting with NAD+ as a cofactor and metabolic enzymes within mitochondria. Its disruption impairs aldehyde detoxification, retinoic acid signaling, and cellular redox balance.
In T-47D breast cancer cells, ALDH1B1 is implicated in maintaining cancer stem cell (CSC) properties, as it confers protection against cytotoxic aldehydes and oxidative stress, thereby supporting clonogenic growth and therapy resistance. Knockout of ALDH1B1 in these polyclonal cells disrupts mitochondrial aldehyde metabolism, leading to accumulation of reactive aldehydes, diminished retinoic acid production, and compromised CSC phenotypes. This sensitizes the cells to chemotherapeutic agents such as doxorubicin or paclitaxel, and reduces sphere-forming capacity, migration, and aldehyde dehydrogenase activity, as measurable by Aldefluor assay. The model thus provides a powerful tool to dissect ALDH1B1-dependent mechanisms in hormone receptor-positive breast cancer and to evaluate novel therapeutic strategies targeting aldehyde dehydrogenase activity.
These polyclonal knockout cells are suited for a broad range of functional assays, including Western blotting and RT-qPCR to confirm protein and transcript level changes, immunofluorescence and flow cytometry for phenotypic characterization, and cell viability or drug sensitivity screens to assess chemoresistance. Migration and sphere formation assays enable interrogation of metastatic and stemness traits. Researchers can explore ALDH1B1??s role in retinoic acid signaling, aldehyde-induced genotoxicity, or metabolic reprogramming in breast cancer. The non-clonal population faithfully models tumor heterogeneity and facilitates pooled CRISPR screens and co-culture studies. For additional details, please contact Ascent Research.
