The TNS1 Knockout U2OS Cell Line is a CRISPR/Cas9-edited cell line in which the TNS1 gene has been disrupted to create a stable loss-of-function model in human U2OS osteosarcoma cells. This product eliminates full-length tensin 1 protein expression, enabling direct assessment of its roles in focal adhesion assembly, cytoskeletal organization, and integrin-mediated signaling pathways without reliance on transient suppression methods.
The parental U2OS cell line is an adherent epithelial-like human osteosarcoma line derived from a 15-year-old female. U2OS cells retain wild-type p53 and functional DNA damage response pathways, making them a widely used model for osteosarcoma biology, p53 signaling, and genomic stability. Their robust growth and reproducible behavior render them highly amenable to stable genetic editing and downstream functional assays, providing a clinically relevant host for interrogating TNS1-driven mechanisms.
Tensin 1 (TNS1) is a focal adhesion scaffold linking integrins (e.g., ITGB1, ITGAV) to the actin cytoskeleton and interacting with PTK2 (FAK), paxillin (PXN), talin-1 (TLN1), vinculin (VCL), and ??-actinin-1 (ACTN1). TNS1 is activated downstream of integrin?CSRC?CILK signaling and regulates RhoA. A critical function is recruitment of PTEN to adhesions, suppressing PI3K/AKT and migration; it also binds DLC1. Loss of TNS1 disrupts adhesion signaling, hyperactivating oncogenic pathways and enhancing motility.
In U2OS cells, TNS1 knockout profoundly alters focal adhesion dynamics and cytoskeletal architecture. Loss of PTEN localization to adhesions elevates basal PI3K/AKT activity, promoting survival and proliferation. Additionally, the absence of TNS1-mediated Rho GTPase regulation increases cell migration and invasion potential. These phenotypic changes recapitulate features of osteosarcoma aggressiveness and provide a tractable model to dissect tumor-suppressive roles of adhesion proteins. The wild-type p53 background further permits investigation of cross-talk between adhesion signaling and genomic stability pathways.
Researchers can employ this knockout cell line in immunofluorescence microscopy to visualize focal adhesion morphology, western blot analysis of phospho-signaling networks, transwell migration and invasion assays, co-immunoprecipitation to probe protein?Cprotein interactions, and quantitative adhesion assays. It is particularly suited for drug testing and mechanistic studies in osteosarcoma and other TNS1-implicated cancers, including breast, prostate, renal, and colorectal carcinomas. This clean genetic ablation enables precise interrogation of integrin-to-cytoskeleton communication and tumor suppression pathways. For further details, please contact Ascent Research.
