Abstract
Previous studies have suggested that 1,9-Pyrazoloanthrone, known as SP600125, can induce cell polyploidization. However, what is the phase of cell cycle arrest caused by SP600125 and the underlying regulation is still an interesting issue to be further addressed. Research in this article shows that SP600125 can block cell cycle progression at the prometaphase of mitosis and cause endomitosis. It is suggested that enhancement of the p53 signaling pathway and weakening of the spindle assembly checkpoint are associated with the SP600125-induced cell cycle arrest. Using preliminary SP600125 treatment, the samples of the cultured fish cells and the fish tissues display a great number of chromosome splitting phases. Summarily, SP600125 can provide a new protocol of chromosomes preparation for karyotype analysis owing to its interference with prometaphase of mitosis.
Highlights
Previous studies showed that SP600125 inhibits cell proliferation in many human cancer cells and in embryonic stem cells by blocking cell cycle progression (Li et al, 2012; Mili et al, 2016; Hai et al, 2019)
Changes of cell proliferation were investigated at the process of SP600125 cyclic treatment by flow cytometry
These results indicated that weakening the activation of p53 can reduce cell cycle arrest in the SP600125-treated fish cells
Summary
Previous studies showed that SP600125 inhibits cell proliferation in many human cancer cells and in embryonic stem cells by blocking cell cycle progression (Li et al, 2012; Mili et al, 2016; Hai et al, 2019). It is reported that effects of the SP600125 on cell cycle arrest are independent of its suppression of JNK activity, and that the knockdown of the jnk gene does not give rise to cell polyploidization (Kim et al, 2010; Zhou et al, 2016). Kim et al (2010) suggested that SP600125 could suppress Cdk and induce endoreplication directly from G2 phase and indirectly inhibited the phosphorylation of Cdk and the persistence of Cdk activity.
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