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

Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated in DADS-induced cell cycle arrest in HL-60 human leukemia cells. Here, we investigated the role of this protein in DADS-induced...

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Veröffentlicht in:	Oncology reports 2012-06, Vol.27 (6), p.1911-1917
Hauptverfasser:	LAN YI, JI, Xiao-Xia, HUI TAN, FENG, Mei-Yan, YI TANG, LING WEN, QI SU
Format:	Artikel
Sprache:	eng
Schlagworte:	Allyl Compounds - pharmacology Antineoplastic Agents - pharmacology Biological and medical sciences CDC2 Protein Kinase - metabolism Cell Cycle Proteins - metabolism Cell Line, Tumor Cell Proliferation Disulfides - pharmacology G2 Phase Cell Cycle Checkpoints - drug effects HL-60 Cells Humans Medical sciences Myeloid Cell Leukemia Sequence 1 Protein Proliferating Cell Nuclear Antigen - metabolism Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism RNA Interference RNA, Small Interfering Tumors
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Zusammenfassung:	Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, we found that myeloid cell leukemia sequence 1 (Mcl1) was downregulated 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 cycle arrest in HL-60 cells. We demonstrated that DADS treatment significantly increased the proportion of G2/M phase HL-60 cells (P
ISSN:	1021-335X 1791-2431
DOI:	10.3892/or.2012.1704