Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells

@article{MurakamiTonami2014InactivationOS,
  title={Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells},
  author={Yuko Murakami-Tonami and Satoshi Kishida and Ichiro Takeuchi and Yuki Katou and John M. Maris and Hitoshi Ichikawa and Yutaka Kondo and Yoshitaka Sekido and Katsuhiko Shirahige and Hiroshi Murakami and Kenji Kadomatsu},
  journal={Cell Cycle},
  year={2014},
  volume={13},
  pages={1115 - 1131}
}
The condensin complex is required for chromosome condensation during mitosis; however, the role of this complex during interphase is unclear. Neuroblastoma is the most common extracranial solid tumor of childhood, and it is often lethal. In human neuroblastoma, MYCN gene amplification is correlated with poor prognosis. This study demonstrates that the gene encoding the condensin complex subunit SMC2 is transcriptionally regulated by MYCN. SMC2 also transcriptionally regulates DNA damage… 
SGO1 is involved in the DNA damage response in MYCN-amplified neuroblastoma cells
TLDR
It is proposed that SGO1 represents a potential molecular target for treatment of MYCN-amplified neuroblastoma and plays a role in the DNA damage response in interphase.
Targeting condensin, a vital spot of MYCN-amplified neuroblastoma
TLDR
In the April 1, 2014 issue of Cell Cycle, Murakami-Tonami et al. reported that downregulation of SMC2, a subunit of condensin, leads to cell death through dysfunction of DNA repair specifically in MYCN-amplified neuroblastoma cells, suggesting thatSMC2 can be an effective anti-cancer target in this type of tumor.
Dangerous liaisons
TLDR
It is demonstrated that SMC2, a condensin core subunit, is regulated by MYCN, a MYC family member, and showed that MYCN amplified tumor cells depend onSMC2 for survival, as these cells undergo massive DNA damage and apoptosis following SMC 2 depletion.
Conditional mutation of Smc5 in mouse embryonic stem cells perturbs condensin localization and mitotic progression
TLDR
Conditional mutation of Smc5 in mouse embryonic stem cells leads to obstruction of chromosome condensation, congression and segregation, accompanied by abnormal spindles, lagging chromosomes and DNA bridges.
Nucleolar protein PES1 is a marker of neuroblastoma outcome and is associated with neuroblastoma differentiation
TLDR
It is shown that NB cases with MYCN amplification and clinically unfavorable stage (INSS stage 4) express higher levels of PES1, a marker of NB outcome, that it regulates NB cell proliferation, and is associated with NB differentiation.
Silencing non-SMC chromosome-associated polypeptide G inhibits proliferation and induces apoptosis in hepatocellular carcinoma cells.
TLDR
Investigation of the significance of non-structural maintenance of chromosomes (non-SMC) chromosome-associated polypeptide G (NCAPG), a subunit of condensin complex I, in the development of hepatocellular carcinoma showed that increased protein expression of NCAPG was found in HCC tissues compared with the matched paracancerous hepatic tissues.
NCAPH promotes cell proliferation and inhibits cell apoptosis of bladder cancer cells through MEK/ERK signaling pathway
TLDR
The results suggest that NCAPH might play an important role in BC progression and provide the potential marker in the diagnosis of BC.
The functional role for condensin in the regulation of chromosomal organization during the cell cycle
TLDR
This review mainly focuses on the molecular mechanisms that condensin uses to exert its functions during the cell cycle progression and discusses the condensIn-mediated chromosomal organization in cancer cells.
Cancer‐associated mutations in the condensin II subunit CAPH2 cause genomic instability through telomere dysfunction and anaphase chromosome bridges
TLDR
In vivo the R551P, R551S, and S556F cancer‐specific CAPH2 mutant proteins are likely to impair condensin II complex formation, impede condens in II activity during mitosis and interphase, and promote genetic heterogeneity in cell populations that can lead to clonal outgrowth of cancer cells with highly diverse genotypes.
Levels of Ycg1 Limit Condensin Function during the Cell Cycle
TLDR
It is demonstrated that Ycg1 levels limit condensin function in interphase cells, and suggested that the association of condens in with chromosomes must be reduced following mitosis to enable efficient progression through the cell cycle.
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