The ITGB1 Knockout 143B Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line. This product features targeted gene disruption of ITGB1, which encodes the integrin ??1 subunit, a central adhesion receptor. The polyclonal format provides a heterogeneous pool of edited cells, offering a robust loss-of-function model while avoiding clonal bias. These cells enable researchers to dissect ??1 integrin-dependent mechanisms in a malignant bone tumor background.
The host cell line, 143B, is an adherent, fibroblastoid cell model originating from a human osteosarcoma. It retains osteoblastic characteristics and is widely employed in studies of osteosarcoma progression and metastasis due to its aggressive in vivo behavior. The cell line’s well-documented signaling and adhesion profiles make it a suitable platform for investigating integrin-mediated oncogenic signaling and evaluating the impact of ITGB1 deletion on tumor cell phenotypes.
Integrin ??1 (CD29) heterodimerizes with various ?? subunits to form receptors for fibronectin, laminin, collagen, and other ECM ligands. Ligand binding triggers recruitment of talin and kindlin-2, which activate integrins and promote assembly of focal adhesions containing FAK, Src, and paxillin. Downstream, FAK activates PI3K-Akt and MAPK-ERK1/2 cascades, while integrin-linked kinase (ILK) and Rho GTPases (RhoA, Rac1) modulate cytoskeletal dynamics. ??1 integrin also interacts with filamin A, vinculin, and tetraspanins (CD9, CD81) to regulate receptor clustering and trafficking. Through these networks, ITGB1 governs cell adhesion, migration, proliferation, and survival, responding to upstream cues such as TGF-??1, EGF, and chemokine receptors.
In the 143B osteosarcoma context, disruption of ITGB1 is expected to compromise ??1 integrin-mediated adhesion and signaling, leading to attenuated FAK phosphorylation and reduced Akt and ERK1/2 activation. This loss-of-function is anticipated to impair anchorage-independent growth, decrease resistance to anoikis, and limit the metastatic potential of these tumor cells. The polyclonal knockout population mimics the genetic heterogeneity found in tumor cell pools, making it particularly relevant for studying the collective impact of ITGB1 loss on tumor progression, drug sensitivity, and invasion without single-clone artifacts.
These polyclonal knockout cells are suitable for a broad range of advanced research applications, including Western blotting and flow cytometry to confirm loss of CD29 surface expression, cell adhesion assays on ECM substrates, transwell migration/invasion assays, and kinetic analysis of FAK or ERK1/2 phosphorylation. They also support anoikis resistance studies and xenograft tumor models to evaluate metastatic behavior and therapeutic responses in vivo. As a versatile tool for exploring integrin signaling in cancer, this product aids investigations into osteosarcoma biology and beyond. For further information or batch-specific inquiries, please contact Ascent Research.
