Effect of Tyrosine Phosphorylation Sites of Oncogenic Protein NPM-ALK on Cell Cycle and Its Related Mechanisms

Lin Lin Hu, Hong Zhen, Xiao Nan Zhang, Li Zhou, Hesham M. Amin, Ping Shi

Research output: Contribution to journalArticlepeer-review

Abstract

UNLABELLED: Objective:To explore the effect of tyrosine phosphorylation sites Tyr644 and Tyr664 in oncogenic protein NPM-ALK on cell cycle and its related mechanisms.

METHODS: Transiently transfected 293T cells and stably transfected Jurkat cells were used for analysis of cell cycle and protein after the transfection with the constructed recombinant plasmid pEGFP-N1, pEGFP-N1-NPM-ALK and pEGFP-N1-NPM-ALK(644, 664); soft agar assay for colony formation was performed to examine the different carcinogenicity of stable cell lines; cell viability of stable cell lines was examined by CCK-8 after the treatment with PPP.

RESULTS: The S arrest occurred in both NPM-ALK(644,664) transfected 293T and Jurkat cells; the susceptibility of NPM-ALK transfected Jurkat cells to PPP was highest among the 3 stable cell lines; the phosphorylated levels of AKT, ERK and STAT3 were decreased in NPM-ALK(644,664) cells compared with the NPM-ALK ones. Additionally, the double mutation induced the increase of CDK2 and the decrease of P27 (P<0.05).

CONCLUSION: The mutation of Tyr644 and 664 sites in NPM-ALK can induce cell cycle arrest in S phase and lower susceptibility to PPP that may be related with the phosphorylation change of cell growth related molecules in the downstream of NPM-ALK.

Original languageEnglish (US)
Pages (from-to)1201-1205
Number of pages5
JournalZhongguo shi yan xue ye xue za zhi
Volume24
Issue number4
DOIs
StatePublished - Aug 1 2016
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine

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