In Stock Cell Lines
Mus musculus (Mouse)
Skin
Adherent
The Igsf11 Knockout B16-F10 Cell Line is a CRISPR/Cas9-edited mouse melanoma model deficient in the tumor suppressor IGSF11. Loss of this homophilic adhesion molecule relieves inhibition of Wnt/??-catenin and ERK/MAPK signaling, upregulating Cyclin D1 and c-Myc. In the aggressive B16-F10 background, this knockout cell line facilitates studies of metastasis, cell adhesion, and pathway regulation. It is suitable for Western blotting, Transwell invasion, tail vein metastasis assays, and epigenetic drug screening. Contact Ascent Research for product inquiries.
Human CD8+ Cytotoxic Killer T Cells
Cat. No. ARP1102
APBB2 Knockout 786-O Polyclonal Cells
Cat. No. ARG24937
BCAT1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG37065
FHL3 Knockout MES-OV Polyclonal Cells
Cat. No. ARG5895
Human Hair Outer Root Sheath Cell Medium
Cat. No. ARM0060
SNU-2535
Cat. No. ARC0862
The Igsf11 Knockout B16-F10 Cell Line is a CRISPR/Cas9-mediated gene disruption product derived from the B16-F10 murine melanoma host. This stable knockout cell line provides a genetically defined model for studying the loss of IGSF11 tumor suppressor function in a highly metastatic background. The cell line is supplied as an established culture suitable for downstream in vitro and in vivo analyses.
The parental B16-F10 cell line, isolated from a C57BL/6 mouse and selected for enhanced lung metastasis, is widely utilized for investigating tumor progression, metastasis, and antitumor immune responses. Its aggressive phenotype and syngeneic nature make it an ideal platform for probing molecular drivers of melanoma dissemination and for preclinical evaluation of therapeutic strategies.
IGSF11 is a homophilic cell adhesion molecule that suppresses proliferation, migration, and invasion by inhibiting Wnt/??-catenin and ERK/MAPK signaling cascades. Its promoter is frequently hypermethylated by DNMT1 and DNMT3A in cancers, leading to epigenetic silencing. Loss of IGSF11 relieves repression of ??-catenin/TCF transcriptional activity, upregulating Cyclin D1 and c-Myc, and simultaneously elevates phospho-ERK1/2 and matrix metalloproteinases. Core pathway components modulated by IGSF11 include Frizzled receptors, Dishevelled, GSK-3??, ??-catenin, TCF/LEF, RAS, RAF, MEK1/2, and ERK1/2.
Knockout of Igsf11 in B16-F10 cells mimics the epigenetic inactivation observed in human melanomas, resulting in enhanced tumorigenicity and metastatic capacity. This engineered system enables dissection of how cell adhesion checkpoints intersect with oncogenic signaling to promote aggressive phenotypes, offering a relevant context for studying the transition from localized to disseminated disease.
The cell line supports a range of research applications, including immunoblotting for IGSF11, ??-catenin, and p-ERK1/2; RT-qPCR quantification of Wnt targets (Axin2, Myc, Ccnd1); and functional assays such as Transwell migration, scratch wound closure, and colony formation. In vivo lung metastasis models via tail vein injection, combined with methylation-specific PCR for Igsf11 promoter analysis and drug response testing, further expand its utility in epigenetic and anti-metastatic drug discovery. For further information, contact Ascent Research.
