Molecular Mechanisms of MYCN Dysregulation in Cancers

Ruochen Liu; Pengfei Shi; Zhongze Wang; Chaoyu Yuan; Hongjuan Cui

doi:10.3389/fonc.2020.625332

Molecular Mechanisms of MYCN Dysregulation in Cancers

Front Oncol. 2021 Feb 3:10:625332. doi: 10.3389/fonc.2020.625332. eCollection 2020.

Authors

Ruochen Liu^{1

2

3}, Pengfei Shi^{1

2

3}, Zhongze Wang^{1

2}, Chaoyu Yuan^{1

2}, Hongjuan Cui^{1

2

3}

Affiliations

¹ State Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass Sciences, Southwest University, Chongqing, China.
² Cancer Center, Reproductive Medicine Center, Medical Research Institute, Southwest University, Chongqing, China.
³ NHC Key Laboratory of Birth Defects and Reproductive Health (Chongqing Key Laboratory of Birth Defects and Reproductive Health, Chongqing Population and Family Planning Science and Technology Research Institute), Chongqing, China.

Abstract

MYCN, a member of MYC proto-oncogene family, encodes a basic helix-loop-helix transcription factor N-MYC. Abnormal expression of N-MYC is correlated with high-risk cancers and poor prognosis. Initially identified as an amplified oncogene in neuroblastoma in 1983, the oncogenic effect of N-MYC is expanded to multiple neuronal and nonneuronal tumors. Direct targeting N-MYC remains challenge due to its "undruggable" features. Therefore, alternative therapeutic approaches for targeting MYCN-driven tumors have been focused on the disruption of transcription, translation, protein stability as well as synthetic lethality of MYCN. In this review, we summarize the latest advances in understanding the molecular mechanisms of MYCN dysregulation in cancers.

Keywords: G-quadruplex; MYCN; NCYM; cancer; gene amplification; super enhancer; synthetic lethality.

Publication types

Review