In Stock Cell Lines
Homo sapiens (Human)
Oral cavity (tongue)
Adherent
The ANGPT1 Knockout CAL-27 Cell Line is a CRISPR/Cas9-edited human cell line lacking angiopoietin-1 expression. Derived from a tongue squamous cell carcinoma lymph node metastasis, CAL-27 cells model aggressive oral cancer. This knockout disrupts Tie2 receptor signaling and downstream PI3K/AKT and MAPK pathways, impairing tumor cell survival and migration. This cell line is ideal for studying angiopoietin-1??s role in oral squamous cell carcinoma angiogenesis, tumor-endothelial crosstalk, and metastasis. Key molecular partners include TEK (Tie2), AKT1, and MAPK1/3. Applications encompass western blot, RT-qPCR, migration and invasion assays, and co-culture with endothelial cells.
Immortalized Human Bronchiole Endothelial Cell
Cat. No. ARI0289
CYR61 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17915
ATG13 Knockout Raji Polyclonal Cells
Cat. No. ARG21294
ASCC2 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28003
DNASE1L1 Knockout 786-O Polyclonal Cells
Cat. No. ARG39367
HAGH Knockout huh-7 Polyclonal Cells
Cat. No. ARG28267
The ANGPT1 Knockout CAL-27 Cell Line is a CRISPR/Cas9-edited human cell line engineered for targeted disruption of the ANGPT1 gene. This gene encodes angiopoietin-1, a secreted glycoprotein that functions as a major ligand for the Tie2 (TEK) receptor tyrosine kinase. The knockout model abolishes angiopoietin-1 expression, providing a clean loss-of-function system for dissecting its roles in tumor biology. Supplied as a ready-to-use cell line, it is suitable for mechanistic studies in cancer and vascular biology.
CAL-27 cells originate from a metastatic lymph node of a patient with tongue squamous cell carcinoma, a highly invasive oral cancer. This cell line is extensively used to model key aspects of tumor progression, including epithelial-to-mesenchymal transition, migration, and invasion. CAL-27 cells retain aggressive phenotypic traits, such as rapid proliferation and enhanced motility, making them a robust platform for studying metastatic mechanisms. Their genetic background and tumorigenic properties render them particularly relevant for investigations into head and neck cancer pathobiology.
Angiopoietin-1 predominantly signals through Tie2, activating downstream PI3K-AKT and MAPK pathways. Key mediators include AKT1, MAPK1/3 (ERK2/1), and the catalytic subunit PIK3CA. Expression of ANGPT1 is regulated by upstream factors such as HIF1A, VEGF-A, TGFB1, and FGF2. Angiopoietin-1 also functionally interacts with integrin ??v??3 and cooperates with VEGF-A to modulate endothelial stability. In the knockout, loss of angiopoietin-1 disrupts Tie2-mediated signaling, thereby impairing AKT and ERK activation.
In CAL-27 cells, endogenously produced angiopoietin-1 may act in an autocrine or paracrine manner to promote tumor cell survival, migration, and crosstalk with the microenvironment. Ablation of ANGPT1 is expected to attenuate these processes, offering a valuable model for studying the tumor-intrinsic functions of angiopoietin-1. This system enables separation of cancer cell-autonomous effects from endothelial-dependent activities, facilitating the dissection of signaling networks that drive oral squamous cell carcinoma progression.
Researchers can employ this cell line in a variety of assays. Western blot and RT-qPCR confirm ANGPT1 knockout at the protein and mRNA levels. Functional readouts include Transwell migration and Matrigel invasion assays to assess metastatic potential. Co-culture with HUVECs in tube formation assays evaluates tumor-endothelial interactions. Transcriptomic analysis via RNA-seq reveals global gene expression changes upon ANGPT1 loss. The line serves as a powerful tool for investigating oral cancer angiogenesis, metastasis, and drug resistance. For detailed product information, contact Ascent Research.
