Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells | Zendy

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Involvement of Mcl1 in diallyl disulfide-induced G2/M cell cycle arrest in HL-60 cells

Author(s) -

Qi Su

Publication year - 2012

Publication title -

oncology reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.094

H-Index - 96

eISSN - 1791-2431

pISSN - 1021-335X

DOI - 10.3892/or.2012.1704

Subject(s) - cell cycle , diallyl disulfide , cell cycle checkpoint , cyclin dependent kinase 1 , proliferating cell nuclear antigen , mcl1 , g1 phase , cell , cell growth , chemistry , microbiology and biotechnology , downregulation and upregulation , cancer research , biology , apoptosis , biochemistry , gene

Diallyl disulfide (DADS) has shown potential as a therapeutic agent in variouscancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) wasdownregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells.Here, we investigated the role of this protein in DADS-induced G2/M cell cyclearrest in HL-60 cells. We demonstrated that DADS treatment significantly increasedthe proportion of G2/M phase HL-60 cells (P<0.05) and caused a time-dependentsignificant downregulation of Mcl1 and the cell cycle-related proteins PCNA andCDK1 (P<0.05). Small interfering RNA-mediated knockdown of Mcl1 expressionin HL-60 cells arrested the cell cycle in G2/M phase. By co-immunoprecipitation,we demonstrated that Mcl1 associated with PCNA and CDK1 in G2/M cell cycle arrestin DADS-treated HL-60 cells. DADS decreased the interaction of Mcl1 with PCNAand CDK1, leading to G2/M cell cycle arrest in HL-60 cells. Mcl1 plays an importantrole in DADS-induced G2/M cell cycle arrest in HL-60 human leukemia cells.

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