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

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

PROVIDER: PRJNA749806 | ENA |

REPOSITORIES: ENA

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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 [MCC26]

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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 [MCC26]

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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: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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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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Comparative Transcriptional Profiling of human Merkel cells and Merkel Cell Carcinoma

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

Comparative Transcriptional Profiling of Human Merkel cells and Merkel Cell Carcinoma

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

Characterization of human Merkel cells and their response to Merkel cell polyomavirus

Project description:Merkel cells are epidermal mechanoreceptor cells responsible for the perception of gentle touch. Merkel cell carcinoma (MCC) is a rare and highly aggressive skin cancer. Although MCC histologically resembles Merkel cells, the cell of origin for MCC is unknown. MCC frequently contains integrated Merkel cell polyomavirus (MCPyV), a small DNA tumor virus with widespread prevalence. Whether MCPyV can transform Merkel cells is unknown. Here, we describe the isolation and long-term expansion of human Merkel cells from neonatal foreskin. We validated the expression of several Merkel cell-related factors by RNASeq, and assessed the ultrastructure by electron microscopy. Culture of Merkel cell preparations on an artificial basement membrane promoted the formation of structures containing both Merkel and non-Merkel cell populations. To determine whether Merkel cells were susceptible to transformation, we expressed tumor-derived MCPyV T antigens and additional oncogenes. We were unable to demonstrate tumorigenesis in immunodeficient mice, but were able to detect T antigen expression from excised cells weeks after implantation. These results highlight that foreskin-isolated Merkel cells can be propagated extensively, sustain expression of MCPyV T antigens, but are not susceptible to transformation by MCPyV, suggesting that Merkel cells from non-glabrous skin may not be a cell of origin for MCC.

2017-04-01 | GSE79657 | GEO

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