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

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

PROVIDER: PRJNA749950 | 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]

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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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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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