MYC: a complex problem

Das, Subhendu; Lewis, Brian A.; Levens, David

doi:10.1016/j.tcb.2022.07.006

Cited by 57 publications

(44 citation statements)

References 111 publications

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“…Of note, MYC binding to Ankrd1 increased during myotube formation (78). Brief Myc overexpression in the soleus did not induce Ankrd1, so MYC may function cooperatively with another factor that is induced during overload to regulate this gene (14,83). To confirm MYC transcription factor binding of myonuclear DNA during mechanical overload, we utilized our RNA-seq data to perform epigenetic Landscape In Silico deletion Analysis (Lisa/Cistrome) (37).…”

Section: Experiments 5: the Myc-controlled Transcriptome In Plantaris...mentioning

confidence: 99%

“…Myc is a transcription factor known to drive cellular plasticity (1,2), epigenetic reprogramming towards stemness as a Yamanaka factor (3)(4)(5)(6), and rapid growth via proliferative and non-proliferative mechanisms (7)(8)(9). A proto-oncogene that dimerizes with MAX and interacts and/or complexes with numerous other proteins (10,11), MYC protein is a "universal amplifier" and "supermanager" of transcription with intricate and multifaceted functionality (12)(13)(14). Evidence for a role of MYC in syncytial muscle fiber growth emerged 20-30 years ago (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

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Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks

Murach¹,

Liu²,

Jude³

et al. 2022

Journal of Biological Chemistry

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Section: Experiments 5: the Myc-controlled Transcriptome In Plantaris...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks

Murach¹,

Liu²,

Jude³

et al. 2022

Journal of Biological Chemistry

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“…USP2-AS1 has been reported to be possibly regulated by MYC [ 27 ]. As a global transcription factor, MYC regulates the expression of a wide range of genes [ 39 ]. It has been reported that MYC helps cells survive under low-oxygen conditions, and emerging evidence suggests that MYC and HIF also cooperate to promote cancer cell growth and progression [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-Regulated lncRNA USP2-AS1 Drives Head and Neck Squamous Cell Carcinoma Progression

Tang

Wang

et al. 2022

Cells

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The role of hypoxia-regulated long non-coding RNA (lncRNA) in the development of head and neck squamous cell carcinoma (HNSCC) remains to be elucidated. In the current study, we initially screened hypoxia-regulated lncRNA in HNSCC cells by RNA-seq, before focusing on the rarely annotated lncRNA USP2 antisense RNA 1 (USP2-AS1). We determined that USP2-AS1 is a direct target of HIF1α and is remarkably elevated in HNSCC compared with matched normal tissues. Patients with a higher level of USP2-AS1 suffered a poor prognosis. Next, loss- and gain-of-function assays revealed that USP2-AS1 promoted cell proliferation and invasion in vitro and in vivo. Mechanically, RNA pulldown and LC–MS/MS demonstrated that the E3 ligase DDB1- and CUL4-associated factor 13 (DCAF13) is one of the binding partners to USP2-AS1 in HNSCC cells. In addition, we assumed that USP2-AS1 regulates the activity of DCAF13 by targeting its substrate ATR. Moreover, the knockdown of DCAF13 restored the elevated cell proliferation and growth levels achieved by USP2-AS1 overexpression. Altogether, we found that lncRNA USP2-AS1 functions as a HIF1α-regulated oncogenic lncRNA and promotes HNSCC cell proliferation and growth by interacting and modulating the activity of DCAF13.

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“…Accordingly, in tumor cells, the promoters of all actively transcribed genes are activated by MYC leading to non-linear amplification of pre-existing transcriptional activities ( 14 ) ( Figure 1 ). The amplifier model also explains how ectopic MYC increases the efficiencies of other transcription factor programs, suggesting that MYC acts as a superior master switch in global transcriptional regulation ( 11 ). Furthermore, recent comprehensive analyses of gene expression revealed that during MYC-initiated tumorigenesis, gene expression changes follow a distinct pattern, which is associated with embryonic, ribosomal biogenesis, and tissue-lineage dedifferentiation processes ( 16 ).…”

Section: Myc: An Oncogenic Transcription Factor With Pleiotropic Func...mentioning

confidence: 99%

“…On the way to achieving a comprehensive view including the dynamics of components regulating MYC-dependent transcription and DNA replication in a quantitative manner, a model has been recently proposed concerning the differential partitioning and trafficking of the largely unstructured MYC protein. In this model, MYC is part of an interaction network between multiple gene–regulatory complexes and factors, thereby energetically modulating the transcriptional process ( 11 ).…”

Section: Myc: An Oncogenic Transcription Factor With Pleiotropic Func...mentioning

confidence: 99%

Strategies to target the cancer driver MYC in tumor cells

Weber

Hartl

2023

Front. Oncol.

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The MYC oncoprotein functions as a master regulator of cellular transcription and executes non-transcriptional tasks relevant to DNA replication and cell cycle regulation, thereby interacting with multiple proteins. MYC is required for fundamental cellular processes triggering proliferation, growth, differentiation, or apoptosis and also represents a major cancer driver being aberrantly activated in most human tumors. Due to its non-enzymatic biochemical functions and largely unstructured surface, MYC has remained difficult for specific inhibitor compounds to directly address, and consequently, alternative approaches leading to indirect MYC inhibition have evolved. Nowadays, multiple organic compounds, nucleic acids, or peptides specifically interfering with MYC activities are in preclinical or early-stage clinical studies, but none of them have been approved so far for the pharmacological treatment of cancer patients. In addition, specific and efficient delivery technologies to deliver MYC-inhibiting agents into MYC-dependent tumor cells are just beginning to emerge. In this review, an overview of direct and indirect MYC-inhibiting agents and their modes of MYC inhibition is given. Furthermore, we summarize current possibilities to deliver appropriate drugs into cancer cells containing derailed MYC using viral vectors or appropriate nanoparticles. Finding the right formulation to target MYC-dependent cancers and to achieve a high intracellular concentration of compounds blocking or attenuating oncogenic MYC activities could be as important as the development of novel MYC-inhibiting principles.

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MYC: a complex problem

Cited by 57 publications

References 111 publications

Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks

Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks

Hypoxia-Regulated lncRNA USP2-AS1 Drives Head and Neck Squamous Cell Carcinoma Progression

Strategies to target the cancer driver MYC in tumor cells

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