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.
GALT Knockout Raji Polyclonal Cells
Cat. No. ARG0910
EPHX1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13224
DEK Knockout A549 Polyclonal Cells
Cat. No. ARG10686
HMCN1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG22551
NFIX Knockout Raji Polyclonal Cells
Cat. No. ARG2041
Mif Knockout 3LL Cell Line
Cat. No. ARG0018
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.
