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MYC S146L is a context-dependent activating substitution in cancer development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE197330 | GEO | 2022/07/31

REPOSITORIES: GEO

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S146L in MYC is a context-dependent activating substitution in cancer development.

Project description:MYC is one of the most dysregulated oncogenes and is thought to be fundamental to tumor formation and/or maintenance in many cancer types. This dominant pro-tumor activity makes MYC an attractive target for cancer therapy. However, MYC is a transcription factor lacking enzymatic activity, and the structure of one of its two domains is unknown e.g., its transactivation domain. Consequently, few direct MYC-targeting therapies have been developed, and none have been successful in the clinic. Nevertheless, significant effort has been devoted to understanding the mechanisms of oncogenic MYC activity with the objective of uncovering novel vulnerabilities of MYC-dependent cancers. These extensive investigations have revealed in detail how MYC translocation, amplification, and other upstream perturbations contribute to MYC activity in cancer. However, missense mutations of the MYC gene have remained relatively understudied for their potential role in MYC-mediated oncogenesis. While the function of several low-frequency mutations in MYC have been described, our understanding of other equally or more frequent mutations is incomplete. Herein, we define the function of a recurrent missense mutation in MYC resulting in the substitution S146L. This mutation enhances the interaction between MYC and its cofactor TRRAP and may enhance oncogenic MYC activity in certain cellular contexts.

| S-EPMC9417018 | biostudies-literature

MYC S146L is a context-dependent activating substitution in cancer development [RNA-seq]

Project description:MYC is one of the most dysregulated oncogenes and is thought to be fundamental to tumor formation and/or maintenance in many cancer types. This dominant pro-tumor activity makes MYC an attractive target for cancer therapy. However, MYC is a transcription factor lacking enzymatic activity, and the structure of one of its two domains is unknown e.g., its transactivation domain. Consequently, few direct MYC-targeting therapies have been developed, and none have been successful in the clinic. Nevertheless, significant effort has been devoted to understanding the mechanisms of oncogenic MYC activity with the objective of uncovering novel vulnerabilities of MYC-dependent cancers. These extensive investigations have revealed in detail how MYC translocation, amplification, and other upstream perturbations contribute to MYC activity in cancer. However, missense mutations of the MYC gene have remained relatively understudied for their potential role in MYC-mediated oncogenesis. While the function of several low-frequency mutations in MYC have been described, our understanding of other equally or more frequent mutations is incomplete. Herein, we define the function of a recurrent missense mutation in MYC resulting in the substitution S146L. This mutation reinforces the interaction between MYC and its cofactor TRRAP and may enhance oncogenic MYC activity in certain cellular contexts. Implication: our results fortify the mechanistic understanding of oncogenic MYC and may indicate a novel prognostic marker for patients whose tumors harbor the somatic mutation resulting in MYC S146L.

2022-07-31 | GSE197323 | GEO

MYC S146L is a context-dependent activating substitution in cancer development [CUT&TAG]

Project description:MYC is one of the most dysregulated oncogenes and is thought to be fundamental to tumor formation and/or maintenance in many cancer types. This dominant pro-tumor activity makes MYC an attractive target for cancer therapy. However, MYC is a transcription factor lacking enzymatic activity, and the structure of one of its two domains is unknown e.g., its transactivation domain. Consequently, few direct MYC-targeting therapies have been developed, and none have been successful in the clinic. Nevertheless, significant effort has been devoted to understanding the mechanisms of oncogenic MYC activity with the objective of uncovering novel vulnerabilities of MYC-dependent cancers. These extensive investigations have revealed in detail how MYC translocation, amplification, and other upstream perturbations contribute to MYC activity in cancer. However, missense mutations of the MYC gene have remained relatively understudied for their potential role in MYC-mediated oncogenesis. While the function of several low-frequency mutations in MYC have been described, our understanding of other equally or more frequent mutations is incomplete. Herein, we define the function of a recurrent missense mutation in MYC resulting in the substitution S146L. This mutation reinforces the interaction between MYC and its cofactor TRRAP and may enhance oncogenic MYC activity in certain cellular contexts. Implication: our results fortify the mechanistic understanding of oncogenic MYC and may indicate a novel prognostic marker for patients whose tumors harbor the somatic mutation resulting in MYC S146L.

2022-07-31 | GSE197327 | GEO

MYC S146L is a context-dependent activating substitution in cancer development

Project description:MYC S146L is a context-dependent activating substitution in cancer development

| PRJNA809750 | ENA

MYC S146L is a context-dependent activating substitution in cancer development [RNA-seq]

Project description:MYC S146L is a context-dependent activating substitution in cancer development [RNA-seq]

| PRJNA809740 | ENA

MYC S146L is a context-dependent activating substitution in cancer development [CUT&TAG]

Project description:MYC S146L is a context-dependent activating substitution in cancer development [CUT&TAG]

| PRJNA809749 | ENA

Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis

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Evolution of Context Dependent Regulation by Expansion of Feast/Famine Regulatory Proteins

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2014-10-03 | E-GEOD-62052 | biostudies-arrayexpress

TRPS1 acts as a context-dependent regulator of mammary epithelial cell growth/differentiation and breast cancer development

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Cav3.2 T-type calcium channel-dependent gene expression after retrieval of context-associated memory

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