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ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MCC26]

ABSTRACT: ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MCC26]

PROVIDER: PRJNA749951 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15257771_1.fastq.gz	Fastqsanger.gz
	SRR15257771_2.fastq.gz	Fastqsanger.gz
	SRR15257772_1.fastq.gz	Fastqsanger.gz
	SRR15257772_2.fastq.gz	Fastqsanger.gz
	SRR15257773_1.fastq.gz	Fastqsanger.gz

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ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY

Project description:ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY

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ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MKL1]

Project description:ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MKL1]

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ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY

Project description:MCCP and MCCN cells are addicted to the oncogenic MUC1-C protein. MUC1-C is a druggable target that may provide new opportunities for advancing MCC treatment.

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ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MCC26]

Project description:MCCP and MCCN cells are addicted to the oncogenic MUC1-C protein. MUC1-C is a druggable target that may provide new opportunities for advancing MCC treatment.

2021-07-30 | GSE180891 | GEO

ADDICTION OF MERKEL CELL CARCINOMA TO MUC1-C IDENTIFIES A POTENTIAL NEW TARGET FOR TREATMENT OF THIS RECALCITRANT MALIGNANCY [MKL1]

Project description:MCCP and MCCN cells are addicted to the oncogenic MUC1-C protein. MUC1-C is a druggable target that may provide new opportunities for advancing MCC treatment.

2021-07-30 | GSE180890 | GEO

MUC1-C IS A MASTER REGULATOR OF SMALL CELL LUNG CANCER PROGRESSION

Project description:Small cell lung cancer (SCLC) is a recalcitrant malignancy associated with dysregulation of MYC signaling and the CDK-RB-E2F axis. We report that expression of the oncogenic MUC1-C protein in SCLC cells integrates activation of MYC and the E2F pathway. MUC1-C drives MYC and E2F target genes and regulates the G2/M checkpoint, mitotic spindle pathway and replication stress response (RSR). We further show that MUC1-C MYC signaling (i) induces NOTCH2, a marker of pulmonary neuroendocrine (NE) stem cells that are the proposed cell of SCLC origin, (ii) drives NE differentiation, as evidenced by expression of ASCL1 and POU3F2/BRN2, and (iii) promotes self-renewal capacity and tumorigenicity of SCLC cells. Analyses of datasets from SCLC tumors confirmed that MUC1 significantly associates with the MYC pathway. These findings uncover a master role for MUC1-C in promoting progression of the SCLC stem cell state and support MUC1-C as a potential target for SCLC treatment.

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MUC1-C IS A MASTER REGULATOR OF SMALL CELL LUNG CANCER PROGRESSION [RNA-seq]

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Project description:Merkel cell carcinoma is supposed to be derived from Merkel cells after infection by Merkel cell polyomavirus (MCV) and other poorly known events. A transcriptional profiling with cDNA microarrays was performed on cells from MCV+ Merkel cell carcinomas and isolated normal Merkel cells. This microarray revealed numerous significantly upregulated genes and down-regulated genes. The extensive list of genes identified in these experiments provides a large body of potentially valuable information of Merkel cell carcinoma carcinogenesis and could represent a source of potential targets for cancer therapy. Two-conditions experiment, MCV vs Normal Merkel Cell. Biological replicates : 4 MCV (Cy5), 1 control = pool of Normal Merkel cells from 3 liftings

2014-01-01 | E-GEOD-50434 | biostudies-arrayexpress

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Project description:Merkel cell carcinoma is supposed to be derived from Merkel cells after infection by Merkel cell polyomavirus (MCPyV) and other poorly known events. A transcriptional profiling with cDNA microarrays was performed on cells from MCPyV(+) Merkel cell carcinomas and isolated normal Merkel cells. This microarray revealed numerous significantly upregulated genes and downregulated genes. The extensive list of genes identified in these experiments provides a large body of potentially valuable information of Merkel cell carcinoma carcinogenesis and could represent a source of potential targets for cancer therapy.

2014-01-01 | GSE50434 | GEO

MUC1-C Drives Lineage Plasticity in Progression to Neuroendocrine Prostate Cancer

Project description:Neuroendocrine prostate cancer (NEPC) is a highly aggressive malignancy of increasing prevalence with an unmet need for targeted therapeutic approaches. The oncogenic MUC1-C protein is overexpressed in castration-resistant prostate cancer (CRPC) and NEPC; however, there is no known role for MUC1-C in driving lineage plasticity to these advanced PC phenotypes. The present studies demonstrate that upregulation of MUC1-C in androgen-independent (AI) PC cells suppresses androgen receptor (AR) axis signaling and induces the neural BRN2 transcription factor by a previously unrecognized MYC-mediated mechanism. MUC1-C activates the BRN2 pathway in association with induction of MYCN, EZH2 and NE differentiation markers (ASCL1, AURKA and SYP), which are linked to NEPC progression. We also show that MUC1-C suppresses the p53 pathway, induces the Yamanaka pluripotency factors (OCT4, SOX2, KLF4 and MYC) and drives stemness. Of potential clinical relevance, targeting MUC1-C decreases PC self-renewal capacity and tumorigenicity, supporting the treatment of CRPC and NEPC with agents directed against this oncoprotein. These findings and the demonstration that MUC1-C is upregulated and associated with suppression of AR signaling, and increases in BRN2 expression and the NEPC score in PC tissues highlight the unanticipated importance of MUC1-C as a master effector of lineage plasticity in progression to advanced PC with NE features.

2019-12-02 | GSE139335 | GEO

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