Reciprocal Induction of MDM2 and MYCN in Neural and Neuroendocrine Cancers.
Reciprocal Induction of MDM2 and MYCN in Neural and Neuroendocrine Cancers.
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MDM2 和 MYCN 在神经和神经内分泌癌中的相互诱导。
DOI：
10.3389/fonc.2020.563156
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发表时间：
2020
影响因子：
4.7
通讯作者：
Cobrinik D
中科院分区：
文献类型：
--
作者：
Tran HN;Singh HP;Guo W;Cambier L;Riggan L;Shackleford GM;Thornton ME;Grubbs BH;Erdreich-Epstein A;Qi DL;Cobrinik D
MYC family oncoproteins MYC, MYCN, and MYCL are deregulated in diverse cancers and via diverse mechanisms. Recent studies established a novel form of MYCN regulation in MYCN-overexpressing retinoblastoma and neuroblastoma cells in which the MDM2 oncoprotein promotes MYCN translation and MYCN-dependent proliferation via a p53-independent mechanism. However, it is unclear if MDM2 also promotes expression of other MYC family members and has similar effects in other cancers. Conversely, MYCN has been shown to induce MDM2 expression in neuroblastoma cells, yet it is unclear if MYC shares this ability, if MYC family proteins upregulate MDM2 in other malignancies, and if this regulation occurs during tumorigenesis as well as in cancer cell lines. Here, we report that intrinsically high MDM2 expression is required for high-level expression of MYCN, but not for expression of MYC, in retinoblastoma, neuroblastoma, small cell lung cancer, and medulloblastoma cells. Conversely, ectopic overexpression of MYC as well as MYCN induced high-level MDM2 expression and gave rise to rapidly proliferating and MDM2-dependent cone-precursor-derived masses in a cultured retinoblastoma genesis model. These findings reveal a highly specific collaboration between the MDM2 and MYCN oncoproteins and demonstrate the origin of their oncogenic positive feedback circuit within a normal neuronal tissue.
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DOI：
10.1146/annurev-pathol-012414-040349
发表时间：
2016-05-23
期刊：
Annual review of pathology
影响因子：
--
作者：
Karni-Schmidt O;Lokshin M;Prives C
通讯作者：
Prives C
影响因子：
56.9
作者：
Jain, M;Arvanitis, C;Felsher, DW
通讯作者：
Felsher, DW
影响因子：
5.8
作者：
Arganda-Carreras, Ignacio;Kaynig, Verena;Seung, H. Sebastian
通讯作者：
Seung, H. Sebastian
影响因子：
10.5
作者：
Fernandez, PC;Frank, SR;Amati, B
通讯作者：
Amati, B
影响因子：
30.8
作者：
Peifer M;Fernández-Cuesta L;Sos ML;George J;Seidel D;Kasper LH;Plenker D;Leenders F;Sun R;Zander T;Menon R;Koker M;Dahmen I;Müller C;Di Cerbo V;Schildhaus HU;Altmüller J;Baessmann I;Becker C;de Wilde B;Vandesompele J;Böhm D;Ansén S;Gabler F;Wilkening I;Heynck S;Heuckmann JM;Lu X;Carter SL;Cibulskis K;Banerji S;Getz G;Park KS;Rauh D;Grütter C;Fischer M;Pasqualucci L;Wright G;Wainer Z;Russell P;Petersen I;Chen Y;Stoelben E;Ludwig C;Schnabel P;Hoffmann H;Muley T;Brockmann M;Engel-Riedel W;Muscarella LA;Fazio VM;Groen H;Timens W;Sietsma H;Thunnissen E;Smit E;Heideman DA;Snijders PJ;Cappuzzo F;Ligorio C;Damiani S;Field J;Solberg S;Brustugun OT;Lund-Iversen M;Sänger J;Clement JH;Soltermann A;Moch H;Weder W;Solomon B;Soria JC;Validire P;Besse B;Brambilla E;Brambilla C;Lantuejoul S;Lorimier P;Schneider PM;Hallek M;Pao W;Meyerson M;Sage J;Shendure J;Schneider R;Büttner R;Wolf J;Nürnberg P;Perner S;Heukamp LC;Brindle PK;Haas S;Thomas RK
通讯作者：
Thomas RK