The BCL2 Knockout 143B Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 143B osteosarcoma cell line, engineered for targeted disruption of the BCL2 gene.
The 143B cell line is a well-established human osteosarcoma model derived from a bone tumor, characterized by its high tumorigenicity and metastatic potential. As a bone cancer cell line of mesenchymal origin, 143B cells exhibit features of malignant osteoblast precursors and are widely utilized in cancer biology studies, including investigations of apoptosis resistance and metastatic mechanisms.
BCL2 encodes a key anti-apoptotic protein that promotes cell survival by binding and sequestering pro-apoptotic effectors BAX and BAK, thereby preventing mitochondrial outer membrane permeabilization (MOMP) and subsequent release of cytochrome c, which is required for apoptosome assembly and caspase-9/3 activation. The expression and activity of BCL2 are tightly controlled by multiple upstream signals: transcription can be induced via NF-??B, STAT3, and MAPK/ERK pathways downstream of cytokines (e.g., IL-6) and growth factors, while PI3K/AKT signaling stabilizes the protein and enhances its anti-apoptotic function. In the intrinsic apoptosis cascade, BCL2 antagonizes the pro-apoptotic BH3-only proteins BAD, BID, BIM, PUMA, and NOXA, which otherwise neutralize BCL2 and enable BAX/BAK oligomerization and MOMP. BCL2 also interacts with other multi-domain BCL2 family members such as BCL-XL and MCL-1, as well as non-homologous partners like BECN1 and IP3R, integrating survival signals with mitochondrial physiology and calcium homeostasis. Thus, BCL2 represents a central regulatory node whose loss disrupts the balance between pro-survival and pro-death signals, unleashing the mitochondrial apoptosis program.
Disruption of BCL2 in the 143B osteosarcoma background eliminates a critical pro-survival checkpoint, potentially sensitizing these cancer cells to intrinsic apoptosis induced by chemotherapeutic agents or targeted BH3 mimetics such as venetoclax. The polyclonal knockout population encompasses a range of editing events, providing a physiologically relevant model for studying the functional consequences of BCL2 loss in a heterogeneous tumor cell milieu.
This product is designed for cancer cell apoptosis studies, drug resistance research, BH3 mimetic sensitivity testing, functional genomics, and target validation. For instance, researchers can evaluate the impact of BCL2 knockout on apoptotic response by performing Annexin V/PI staining and caspase-3/9 activity assays, or assess mitochondrial outer membrane permeabilization via cytochrome c release and JC-1 staining. Additionally, co-immunoprecipitation and BH3 profiling can be employed to map altered BCL2 family protein interactions and mitochondrial priming states. For technical inquiries and ordering information, please contact Ascent Research.
