6,7-di-O-acetylsinococuline (FK-3000) induces G2/M phase arrest in breast carcinomas through p38 MAPK phosphorylation and CDC25B dephosphorylation | Zendy

Yongchun Li | Zendy; Bong-Hee Kim | Zendy; Soon-Chang Cho | Zendy; MiAe Bang | Zendy; Sunmin Kim | Zendy; Dae-Hun Park | Zendy

Open Access

6,7-di-O-acetylsinococuline (FK-3000) induces G2/M phase arrest in breast carcinomas through p38 MAPK phosphorylation and CDC25B dephosphorylation

Author(s) -

Yongchun Li,

Bong-Hee Kim,

Soon-Chang Cho,

MiAe Bang,

Sunmin Kim,

Dae-Hun Park

Publication year - 2014

Publication title -

international journal of oncology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.405

H-Index - 122

ISSN - 1019-6439

DOI - 10.3892/ijo.2014.2739

Subject(s) - dephosphorylation , biology , phosphorylation , cancer research , molecular medicine , cell cycle , oncogene , apoptosis , mapk/erk pathway , microbiology and biotechnology , biochemistry , phosphatase

We evaluated the cytostatic effect of 6,7-di-O-acetyl-sinococuline (FK-3000) isolated from Stephania delavayi Diels. against breast carcinoma cell lines MDA-MB‑231 and MCF-7. FK-3000 suppressed CDC25B phosphorylation directly and indirectly via p38 MAPK phosphorylation. CDC25B dephosphorylation decreased levels of cyclin B and phospho-CDC-2, and ultimately induced cell cycle arrest at the G2/M phase. The p38 MAPK inhibitor, SB 239063 blocked FK-3000-induced p38 MAPK phosphorylation and nuclear accumulation, but did not completely rescue cell death. Conclusively FK-3000 exerts its antiproliferative effect through two pathways: i) G2/M cell cycle arrest via downregulation of cyclin B and phospho-CDC2 by p38 MAPK phosphorylation and CDC25B dephosphorylation, and ii) p38 MAPK-independent induction of apoptosis.

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