In Stock Cell Lines
Homo sapiens (Human)
Skin
Adherent
The FOSL1 Knockout HaCaT Cell Line is a CRISPR/Cas9-edited human keratinocyte line that eliminates expression of Fra-1, a crucial component of the AP-1 transcription factor complex. Fra-1 is activated by ERK1/2 downstream of EGFR and TGF-??, and it transcriptionally regulates MMP1, MMP9, and EMT drivers such as ZEB1 and SNAI1, linking it to key processes in cancer and skin biology. This knockout model supports investigations into AP-1-mediated proliferation, migration, and invasion, with direct relevance to cutaneous squamous cell carcinoma, psoriasis, and wound healing. Applications include scratch assays, Transwell migration, drug screening, and transcriptomic profiling, offering a reliable platform for dissecting Fra-1 function in keratinocytes.
GNAI1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16934
MTHFS Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16856
HERC1 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24522
JAG2 Knockout UMUC-3 Polyclonal Cells
Cat. No. ARG36946
IDO1 Knockout T47D Polyclonal Cells
Cat. No. ARG36800
LY96 Knockout KYSE30 Polyclonal Cells
Cat. No. ARG9688
The FOSL1 Knockout HaCaT Cell Line is a CRISPR/Cas9-edited human knockout cell line designed to abrogate expression of the Fra-1 transcription factor through targeted disruption of the FOSL1 locus. This model provides a stable loss-of-function system in a keratinocyte background, enabling dissection of AP-1-dependent gene regulatory networks without the confounding effects of pharmacological inhibition.
The parental HaCaT cell line is a spontaneously immortalized, aneuploid, non-tumorigenic human keratinocyte line derived from adult skin. HaCaT cells retain the capacity for epidermal differentiation and are widely used to study barrier formation, wound healing, and cutaneous homeostasis. Their responsiveness to growth factors and cytokines makes them a robust platform for investigating skin biology and disease-relevant signaling.
FOSL1 (Fra-1) is a core component of the AP-1 transcription factor complex, heterodimerizing with JUN family members (c-Jun, JunB, JunD) and ATF proteins. Fra-1 is activated by ERK1/2 (MAPK3/1) downstream of EGFR in response to EGF or TGF-??, and its transcription is controlled by SRF/ELK1 and Wnt/??-catenin?CTCF/LEF. Once activated, Fra-1?CAP-1 dimers drive expression of matrix metalloproteinases (MMP1, MMP9), pro-migratory factors (ITGB3, CYR61), EMT regulators (ZEB1, SNAI1, VIM, CDH2), and the cell-cycle gene CCND1. Fra-1 interacts with p300/CBP and SMAD3, integrating TGF-?? and chromatin-remodeling signals. Knockout of FOSL1 eliminates this transcriptional hub, disarming AP-1 programs for proliferation, invasion, and survival.
In the HaCaT keratinocyte context, loss of FOSL1 profoundly alters cellular responses to mitogenic and pro-inflammatory stimuli. The absence of Fra-1 disrupts the orchestration of genes required for re-epithelialization and ECM remodeling during wound healing, impairs migration and invasiveness in scratch and Transwell assays, and attenuates the expression of EMT-associated markers. Because Fra-1 is frequently overexpressed in cutaneous squamous cell carcinoma and other epithelial cancers, the FOSL1 Knockout HaCaT Cell Line serves as a critical tool to distinguish Fra-1-dependent from Fra-1-independent effects in hyperproliferative and invasive phenotypes. It also enables the study of AP-1 involvement in inflammatory skin diseases such as psoriasis, where Fra-1 potentiates cytokine-driven keratinocyte hyperproliferation.
This knockout line is suited for studying AP-1-driven tumor invasion, EMT, and wound healing. It supports drug screening against AP-1/MAPK/ERK targets, dermatological toxicity testing, and transcriptomic profiling of the Fra-1 network. Assays include immunoblotting for Fra-1/MMPs/EMT markers, RT-qPCR, scratch/Transwell migration, immunofluorescence for keratins, AP-1 luciferase reporter, RNA-seq, and apoptosis analysis. For more details, contact Ascent Research.
