The CD109 Knockout MES-OV Polyclonal Cells constitute a CRISPR/Cas9-mediated polyclonal knockout cell population in which the CD109 gene has been disrupted within the human ovarian clear cell carcinoma cell line MES-OV. This product provides a heterogeneous pool of edited cells, each carrying targeted disruptions in CD109, enabling loss-of-function studies without clonal selection. As a polyclonal knockout model, it retains the genetic diversity of the parental line while systematically ablating CD109 expression, thereby serving as a robust platform for investigating CD109-dependent phenotypes in a cancer-relevant background.
MES-OV is a human ovarian clear cell carcinoma cell line derived from a patient tumor, representing a clinically aggressive subtype of epithelial ovarian cancer. Clear cell carcinoma is characterized by distinct molecular features, including frequent ARID1A mutations, and is associated with poor prognosis and chemoresistance. As an established model for ovarian clear cell carcinoma, MES-OV cells preserve key oncogenic pathways and tumorigenic properties, making them suitable for dissecting signaling mechanisms that drive tumor progression, metastasis, and drug resistance in this specific histological context.
CD109 encodes a glycosylphosphatidylinositol (GPI)-anchored cell surface glycoprotein that functions as a TGF-?? co-receptor and negative regulator of TGF-?? signaling. Mechanistically, CD109 sequesters TGF-?? ligands such as TGF-??1, thereby preventing their interaction with the TGF-?? receptor complexes TGFBR1 and TGFBR2. This ligand trapping attenuates downstream SMAD2/3 phosphorylation and nuclear translocation, leading to reduced transcriptional activation of target genes including SMAD7, PAI-1, and CTGF. Additionally, CD109 modulates non-canonical pathways, intersecting with STAT3, JAK/STAT, PI3K/AKT, and MAPK/ERK signaling cascades. Upstream, CD109 expression is induced by TGF-?? itself, as well as by EGF, IL-6, and hypoxic conditions, establishing feedback loops that fine-tune cellular responses. The loss of CD109 disrupts this inhibitory control, potentially unleashing TGF-??-driven transcriptional programs and crosstalk with other pro-tumorigenic pathways.
In the MES-OV ovarian clear cell carcinoma background, CD109 disruption is expected to enhance TGF-?? responsiveness, thereby altering cell behaviors central to cancer progression. Given that TGF-?? can exert dual roles??acting as a tumor suppressor in early stages and a promoter of invasion and metastasis in advanced disease??the CD109 knockout model enables dissection of context-dependent signaling outcomes. Enhanced SMAD2/3 and STAT3 activation, coupled with elevated expression of MMPs and PAI-1, may drive increased migration, invasion, and epithelial-mesenchymal transition. This model is therefore particularly relevant for studying mechanisms of ovarian cancer metastasis, therapeutic resistance, and the contribution of TGF-?? signaling in clear cell carcinoma aggressiveness.
Researchers can employ the CD109 Knockout MES-OV Polyclonal Cells in a wide array of experimental applications, including quantitative assessment of TGF-?? pathway activity, functional migration and invasion assays, proliferation studies, and genome-wide expression profiling via RNA-seq. Validation of CD109 deletion can be performed by Western blotting or immunofluorescence, while downstream signaling alterations are detectable through phospho-SMAD2/3 immunoblotting and RT-qPCR analysis of TGF-?? target genes. Co-immunoprecipitation studies can further elucidate altered receptor-ligand interactions in the absence of CD109. These applications facilitate investigations into TGF-?? biology, ovarian cancer biology, drug resistance mechanisms, and biomarker discovery. For further information, please contact Ascent Research.
