The BIN1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 human colorectal adenocarcinoma cells, with disruption of the BIN1 tumor suppressor gene. This loss-of-function model facilitates investigation of BIN1 in apoptosis, endocytosis, and cell cycle regulation. The polyclonal format avoids clonal selection bias, representing a heterogeneous gene-edited pool for more physiologically relevant studies.
The HT29 cell line is an epithelial model from human colorectal adenocarcinoma. It undergoes enterocytic differentiation under specific conditions, widely used for intestinal epithelial biology and colorectal cancer research. HT29 cells contain mutations in APC and p53, offering a relevant genetic background for studying tumor suppressors like BIN1, and are valued for their well-characterized signaling networks.
BIN1 is a tumor suppressor with dual roles: it interacts with and inhibits the oncogenic transcription factor c-Myc, promoting apoptosis and cell cycle arrest, and it acts in clathrin-mediated endocytosis by recruiting dynamin 2 and amphiphysin for membrane scission. Upstream regulators include c-Myc, E2F1, and p53; downstream, BIN1 inhibits c-Myc, activates caspase-3, and upregulates p21. Interacting partners such as clathrin and endophilin A1 highlight its central position in coordinating tumor suppression and membrane trafficking.
In the HT-29 colorectal cancer context, BIN1 disruption enables dissection of its tumor suppressor mechanisms, particularly how loss of Myc inhibition and endocytic regulation promotes malignancy. This model addresses the interaction between BIN1 loss and colorectal cancer-specific genetic alterations, aiding studies of apoptosis evasion, genomic instability, and aberrant trafficking.
This knockout model supports diverse applications: apoptosis assays (Annexin V/PI, caspase activity), Myc reporter assays, endocytosis measurements (transferrin uptake), and proliferation, migration, and invasion analyses (MTT, Transwell). Drug sensitivity studies using 5-fluorouracil explore chemoresistance. Molecular endpoints are validated by Western blotting, RT-qPCR, and Sanger sequencing. For further inquiries, contact Ascent Research.
