MYCN and Metabolic Reprogramming in Neuroblastoma.
MYCN and Metabolic Reprogramming in Neuroblastoma.
复制标题
MYCN与神经母细胞瘤中的代谢重编程
DOI:
10.3390/cancers14174113
复制
发表时间:
2022-08-25
期刊:
影响因子:
5.2
通讯作者:
Ding, Han-Fei
中科院分区:
文献类型:
--
作者:
Bansal, Mohit;Gupta, Anamika;Ding, Han-Fei
Metabolic reprogramming has a central role in the initiation and progression of cancer, including high-risk neuroblastoma, a deadly childhood malignant tumor of the sympathetic nervous system. This rewiring of cellular metabolism increases the manufacture of fuel and building blocks for biomass production, which is essential to sustain the growth and proliferation of neuroblastoma cells. However, the rewiring also makes neuroblastoma cells metabolically distinct from normal sympathetic neurons, thereby offering new therapeutic opportunities. In this review, we summarize the recent progress in the study of neuroblastoma metabolic reprogramming and underlying molecular mechanisms. Neuroblastoma is a pediatric cancer responsible for approximately 15% of all childhood cancer deaths. Aberrant MYCN activation, as a result of genomic MYCN amplification, is a major driver of high-risk neuroblastoma, which has an overall survival rate of less than 50%, despite the best treatments currently available. Metabolic reprogramming is an integral part of the growth-promoting program driven by MYCN, which fuels cell growth and proliferation by increasing the uptake and catabolism of nutrients, biosynthesis of macromolecules, and production of energy. This reprogramming process also generates metabolic vulnerabilities that can be exploited for therapy. In this review, we present our current understanding of metabolic reprogramming in neuroblastoma, focusing on transcriptional regulation as a key mechanism in driving the reprogramming process. We also highlight some important areas that need to be explored for the successful development of metabolism-based therapy against high-risk neuroblastoma.
登录
查看更多内容
影响因子:
50.3
作者:
Carroll PA;Diolaiti D;McFerrin L;Gu H;Djukovic D;Du J;Cheng PF;Anderson S;Ulrich M;Hurley JB;Raftery D;Ayer DE;Eisenman RN
通讯作者:
Eisenman RN
影响因子:
6
作者:
Alam, Goleeta;Cui, Hongjuan;Ding, Han-Fei
通讯作者:
Ding, Han-Fei
影响因子:
22.7
作者:
Alborzinia, Hamed;Florez, Andres F.;Kreth, Sina;Brueckner, Lena M.;Yildiz, Umut;Gartlgruber, Moritz;Odoni, Dorett, I;Poschet, Gernot;Garbowicz, Karolina;Shao, Chunxuan;Klein, Corinna;Meier, Jasmin;Zeisberger, Petra;Nadler-Holly, Michal;Ziehm, Matthias;Paul, Franziska;Burhenne, Juergen;Bell, Emma;Shaikhkarami, Marjan;Wuerth, Roberto;Stainczyk, Sabine A.;Wecht, Elisa M.;Kreth, Jochen;Buettner, Michael;Ishaque, Naveed;Schlesner, Matthias;Nicke, Barbara;Stresemann, Carlo;Llamazares-Prada, Maria;Reiling, Jan H.;Fischer, Matthias;Amit, Ido;Selbach, Matthias;Herrmann, Carl;Woelfl, Stefan;Henrich, Kai-Oliver;Hoefer, Thomas;Trumpp, Andreas;Westermann, Frank
通讯作者:
Westermann, Frank
影响因子:
56.9
作者:
BRODEUR, GM;SEEGER, RC;BISHOP, JM
通讯作者:
BISHOP, JM
DOI:
10.1016/j.biocel.2007.01.020
发表时间:
2008-01-01
影响因子:
4
作者:
Ameri, Kurosh;Harris, Adrian L.
通讯作者:
Harris, Adrian L.