In Stock Cell Lines
Homo sapiens (Human)
Skin
Adherent
The MELTF Knockout SK-MEL-28 Cell Line is a CRISPR/Cas9-edited human melanoma line with targeted disruption of the MELTF gene. MELTF (p97) is a multifunctional protein involved in iron metabolism and plasminogen activation, promoting melanoma cell proliferation and migration through downstream MMP2/MMP9 activation and FAK/AKT signaling. Loss of MELTF in the SK-MEL-28 background impairs invasion, matrix remodeling, and survival pathways, providing a relevant model for melanoma metastasis research. This knockout line is suitable for assays such as migration/invasion, MMP activity measurement, and phospho-signaling analysis, supporting drug target validation and anti-melanoma screening.
NME7 Knockout A2780 Polyclonal Cells
Cat. No. ARG18852
HIC1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG22518
AP3S2 Knockout jurkat Polyclonal Cells
Cat. No. ARG33854
MISP Knockout Raji Polyclonal Cells
Cat. No. ARG1869
Chicken Small Intestinal Mucosal Epithelial Cells
Cat. No. ARP0969
ARID1A Knockout HeLa Cell Line
Cat. No. ARG0336
The MELTF Knockout SK-MEL-28 Cell Line is a CRISPR/Cas9-edited human cell line enabling loss-of-function studies of the MELTF gene. Created via CRISPR/Cas9-mediated gene disruption in the SK-MEL-28 melanoma background, this model provides a stable platform to investigate MELTF ablation. It is suited for advanced research in cancer biology, signal transduction, and drug discovery.
The parental SK-MEL-28 cell line is a human malignant melanocytic tumor cell line originating from a male patient with malignant melanoma. It is widely used as an in vitro melanoma model, exhibiting dysregulated proliferation and migration characteristic of metastatic disease. SK-MEL-28 cells are responsive to key oncogenic pathways, including BRAF/MEK/ERK signaling, and are instrumental in melanoma and drug response studies.
MELTF (p97) functions in iron binding and transport and critically regulates the plasminogen activation system. It binds plasminogen, promoting its conversion to plasmin, which then activates matrix metalloproteinases MMP2 and MMP9 to degrade the extracellular matrix, facilitating invasion and migration. MELTF also affects downstream focal adhesion kinase (FAK) and AKT survival signaling, while being regulated by the MITF transcription factor and the BRAF/MEK/ERK cascade. Knockout of MELTF disrupts these interactions, attenuating MAPK and AKT signaling, impairing plasminogen activation and matrix remodeling, and reducing the iron-handling capability of cells.
In the SK-MEL-28 melanoma background, loss of MELTF significantly impairs proliferation, migration, and invasive capacity. The knockout model reveals how MELTF-driven iron homeostasis and plasmin-mediated ECM degradation contribute to melanoma aggression. It is an effective tool for dissecting the roles of MELTF in focal adhesion dynamics, integrin signaling, and crosstalk with the uPA/uPAR/plasmin system, as well as for studying its interactions with LRP1 and heparan sulfate proteoglycans.
This cell line supports diverse research applications, including melanoma metastasis studies, target validation, and anti-melanoma compound screening. Typical assays include Western blot for MELTF and downstream targets, Boyden chamber migration/invasion, gelatin zymography for MMP activity, phospho-ERK/AKT analysis, and iron uptake measurements. Additional techniques such as RT-qPCR, cell proliferation assays, and immunofluorescence for focal adhesions can be employed. For further information, please contact Ascent Research.
