The ASGR1 Knockout MCF-7 Polyclonal Cells product provides a heterogeneous population of MCF-7 cells in which the ASGR1 gene has been disrupted by CRISPR/Cas9-mediated gene editing. This polyclonal knockout cell pool is generated without single-cell cloning, preserving natural genetic heterogeneity while eliminating functional ASGR1 expression across the population. The use of a polyclonal format minimizes clonal selection artifacts and offers a more representative model of gene loss in a bulk cell population, suitable for functional genomics and drug discovery applications.
MCF-7 is a widely utilized human breast adenocarcinoma cell line originally derived from the pleural effusion of a 69-year-old female with metastatic disease. These cells are estrogen receptor (ER)-positive, progesterone receptor (PR)-positive, and serve as a canonical model of hormone-responsive luminal breast cancer. MCF-7 cells have been extensively characterized for their dependence on estrogen for growth and their sensitivity to anti-estrogen therapies, making them a central tool for studying ER signaling, endocrine resistance, and metastatic progression.
The ASGR1 gene encodes the major subunit of the asialoglycoprotein receptor, a transmembrane lectin that recognizes galactose-terminal glycans on desialylated glycoproteins. Ligand binding triggers clathrin-mediated endocytosis, involving AP2M1, CLTC, and DNM2 for vesicle scission, and trafficking through RAB5A-positive endosomes to LAMP1-positive lysosomes. Although predominantly hepatocytic, ASGR1 is expressed in MCF-7 breast cancer cells. Transcription is regulated by HNF4A, HNF1A, and C/EBP??. Downstream, ASGR1 internalization can modulate the MAPK pathway, linking endocytosis to proliferation signaling.
In MCF-7 cells, ASGR1 knockout enables dissection of how glycoprotein clearance intersects with ER signaling in luminal breast cancer. Altered glycosylation is a cancer hallmark, and ASGR1 may influence receptor stability and MAPK activation. The polyclonal knockout population avoids clonal artifacts, providing a robust tool for evaluating ASGR1??s role in proliferation and endocytic trafficking.
This ASGR1 knockout model supports diverse research applications, including glycoprotein trafficking assays using labeled asialo-orosomucoid, drug conjugate internalization studies exploiting galactose-recognition, and investigation of MAPK pathway modulation. Standard techniques such as Western blotting, RT-qPCR, and immunofluorescence can confirm knockout and assess downstream signaling, while flow cytometry and endocytosis assays quantitatively measure ligand uptake. Proliferation assays under varying estrogen conditions reveal the impact of ASGR1 loss on cell growth. For further details, please contact Ascent Research.
