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RNA-seq profiling of PRAME knockdown in A375SM skin cutaneous melanoma cells

ABSTRACT: This study investigates the transcriptomic effects of PRAME knockdown in the A375SM skin cutaneous melanoma cell line. Cells were transduced with either control shRNA (shCtrl) or PRAME-targeting shRNA (shPRAME), followed by paired-end RNA sequencing. The dataset provides gene expression changes associated with PRAME silencing and offers insights into PRAME-regulated pathways in melanoma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE311500 | GEO | 2025/12/31

REPOSITORIES: GEO

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Transcriptome profiling of A375SM melanoma cells following PRAME and BAP1 knockdown

Project description:To investigate the transcriptomic changes associated with PRAME and BAP1 knockdown, RNA-seq was performed on A375SM melanoma cells stably expressing shRNA targeting PRAME (shPRAME), BAP1 (shBAP1), or a non-targeting control (shEmpty). This study aims to understand the role of PRAME and BAP1 in gene regulation and melanoma progression.

2025-09-02 | GSE306132 | GEO

The Influence of Melanoma Extracellular Vesicles on Benign Melanocytes: A Role for PRAME in Modulation of the Tumor Microenvironment

Project description:This study investigates the role of PRAME (Preferentially Expressed Antigen in Melanoma), a cancer-testis antigen, in melanoma progression, particularly its function in melanoma-derived extracellular vesicles (EVs) and its impact on benign primary melanocytes.

2024-10-16 | GSE279329 | GEO

PRAME-mediated retinoid resistance in keratinocyte carcinomas is overcome by EZH2 inhibition

Project description:Preferentially Expressed Antigen of Melanoma (PRAME) is a cancer-testis antigen that is expressed in subsets of basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC), collectively termed keratinocyte carcinomas (KC). PRAME functions as a transcriptional co-repressor of retinoid signaling by guiding enhancer of zeste homologue 2 (EZH2), a repressive histone methyltransferase, to retinoic acid response elements (RARE) found in gene promoters. The functions and therapeutic relevance of PRAME expression in KC have not been investigated. In the present study, we evaluated the implications of PRAME expression upon KC development and response to retinoid-based therapeutics. High PRAME expression in tumors was negatively correlated with epidermal differentiation gene signatures. Similarly, PRAME overexpression (OE) downregulated epidermal differentiation gene signatures, and impaired epidermal differentiation. PRAME OE also attenuated retinoid-induced RARE activation, growth suppression and differentiation responses. Conversely, low-PRAME tumors and PRAME-depleted KC cells possessed enrichment of epidermal differentiation gene signatures. PRAME depletion also restored retinoid-induced RARE activation, suppression of KC growth, keratinization suppression in SCC cells and cell death signaling in BCC cells. Furthermore, EZH2 inhibitors potentiated the retinoid-induced RARE activation and suppress the growth of PRAME-expressing BCC and cSCC cells. We demonstrate that PRAME confers retinoid resistance in KC, and we contend that PRAME-mediated retinoid resistance in KC may be overcome by targeting EZH2.

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Gene expression profiling of PRAME-positive and PRAME-negative osteosarcoma samples

Project description:Preferentially Expressed Antigen in Melanoma (PRAME) is frequently overexpressed in a wide variety of cancers and it has been proposed as prognostic marker for clinical outcome. It belongs to a class of non-mutated genes whose expression seems to be mostly restricted to tumor cells. Osteosarcoma is the most common primary malignant bone tumor in children and young adults. Despite advances in the diagnosis and management of osteosarcoma, long-term survival has not envolved substantially in the past decades, justifying efforts in finding effective therapeutic targets. In order to assess transcriptome characteristics that could contribute to further comprehend PRAME association with cancer, the technique of gene expression profiling was used to compare PRAME-positive and PRAME-negative osteosarcoma samples. Keywords: disease state analysis Six tumor samples representing distinct histological classes of osteosarcoma (telangiectatic, giant cell, anaplastic, osteoblastic and chondroblastic) were included in this study. They were obtained from individual patients ranging from 5 to 29 years old. Microarray experiments were carried out using the microarray platform CodeLink (GE Healthcare). This platform utilizes bioarrays consisting of 30-base, single pre-validated oligonucleotide probe per gene target. CodeLink UniSet Human I bioarrays, containing 10,000 human transcripts, were used for all experiments. Hybridization procedures strictly followed protocols provided by the manufacturer (GE Healthcare). A total of 12 arrays were hybridized, including 6 tumor samples (3 PRAME-positive and 3 PRAME-negative) and their respective technical replicates. Arrays were scanned following the recommended scanning procedure and settings for use with CodeLink bioarrays (GE Healthcare) on GenePix 4000B Array Scanner/GenePix Pro 4.0 software (Axon Instruments).

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Gene expression associated with lentiviral expression of PRAME in normal hematopoietic progenitors.

Project description:To identify gene expression that distinguishes hematopoietic cells that express PRAME from those that do not, normal CD34+ cells with forced PRAME expression were compared to cells without PRAME expression in culture over time (days 4, 7, 14) using Affymetrix HU-133A microarrays Normal CD34+ progenitor cells not expressing PRAME were transduced with either PRAME cDNA (no 3' utr) or a corresponding empty vector control by lentiviral vector infection. Two replicates were performed for each condition (PRAME and control) at three experimental time points (days 4, 7, and 14 in culture). A single-stranded linear amplification protocol was used to process total RNA (one microgram) for the microarrays. This protocols is described in detail in PMID 14706461.

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The tumor antigen PRAME is a substrate recognition subunit of a Cul2-based ubiquitin ligase and is associated with active NFY promoters

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PRAME induces genomic instability in uveal melanoma

Project description:PRAME induces genomic instability in uveal melanoma

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Gene expression profile of Hodgkin’s lymphoma cells after knock-down of PRAME

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2012-12-21 | GSE40988 | GEO

The tumor antigen PRAME is a substrate recognition subunit of a Cul2-based ubiquitin ligase and is associated with active NFY promoters

2011-07-29 | E-GEOD-26439 | biostudies-arrayexpress

The influence of melanoma extracellular vesicles on benign melanocytes, dermal fibroblasts and microvascular endothelial cells (part1)

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