In Stock Cell Lines
Homo sapiens (Human)
Skin
Adherent
CRISPR/Cas9-edited JPX knockout in the A-375 human melanoma cell line. This model disrupts the JPX lncRNA, which recruits CTCF and PRC2 to activate XIST transcription and propagate X-chromosome inactivation through H3K27me3 deposition. It provides a clean background to study how pluripotency factors (OCT4, SOX2, NANOG) intersect with epigenetic silencing. Ideal for investigating X-inactivation mechanisms, lncRNA biology, and epigenetic dysregulation in melanoma. Validated for RNA FISH, RIP, ChIP-qPCR, RT-qPCR, and proliferation assays. Enables elucidation of JPX??s role in cancer cell fitness and chromatin modification.
Immortalized Mouse Carotid Artery Endothelial Cell
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EFHD1 Knockout Raji Polyclonal Cells
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BTN2A1 Knockout HAP1 Polyclonal Cells
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The JPX Knockout A-375 Cell Line is a CRISPR/Cas9-edited knockout cell line that disrupts the JPX long non-coding RNA (lncRNA) gene, a critical activator of XIST transcription and X-chromosome inactivation. This loss-of-function model enables dissection of JPX-dependent epigenetic silencing without introducing exogenous sequences. Generated via CRISPR/Cas9-mediated gene disruption, the line provides a genetically defined background to study lncRNA-mediated regulation of chromatin and gene expression. It is supplied as a proliferating cell line, ready for experiments examining the functional consequences of JPX ablation on XIST expression, PRC2 recruitment, and H3K27me3 deposition.
The A-375 host cell line originates from a primary cutaneous malignant melanoma of a 54-year-old female. These adherent cells retain hallmark features of aggressive melanoma, including rapid growth and metastatic gene signatures. A-375 is a well-established model for investigating oncogenic signaling, epigenetic dysregulation, and therapeutic responses in melanoma. Its human origin and tumorigenic background make it ideal for exploring how lncRNAs like JPX modulate cancer-relevant epigenetic programs and cellular phenotypes.
JPX acts mechanistically by binding the insulator protein CTCF and recruiting polycomb repressive complex 2 (PRC2) to the XIST promoter. This interaction catalyzes trimethylation of histone H3 at lysine 27 (H3K27me3), initiating XIST transcription and spreading of X-chromosome inactivation. Upstream, pluripotency transcription factors OCT4, SOX2, and NANOG regulate JPX expression, linking developmental cues to epigenetic silencing. The JPX?CCTCF?CPRC2?CXIST axis thus orchestrates large-scale chromatin remodeling, with JPX serving as a scaffold for silencing complex assembly.
In melanoma, aberrant lncRNA expression can rewire epigenetic landscapes to promote proliferation and survival. Because JPX lies upstream of XIST, its knockout in A-375 cells permits direct assessment of XIST-dependent and -independent roles in malignant phenotypes. Loss of JPX may alter H3K27me3 distribution beyond the X chromosome, affecting gene networks relevant to melanoma progression. This model can reveal whether JPX contributes to tumor cell fitness through canonical X-inactivation pathways or through alternative mechanisms involving PRC2 recruitment to autosomal targets.
This cell line is suited to a broad array of experimental approaches. RNA fluorescence in situ hybridization (RNA FISH) visualizes XIST localization; RNA immunoprecipitation (RIP) profiles JPX?CCTCF or JPX?CPRC2 interactions; chromatin immunoprecipitation quantitative PCR (ChIP-qPCR) measures H3K27me3 occupancy at the XIST locus; RT-qPCR quantifies XIST transcript levels; and proliferation assays evaluate functional effects. Together, these tools enable rigorous investigation of lncRNA-driven epigenetic regulation in cancer. For further technical information, please contact Ascent Research.
