Sulforaphane induced cell cycle arrest in the G2/M phase via the blockade of cyclin B1/CDC2 in human ovarian cancer cells.
Sulforaphane induced cell cycle arrest in the G2/M phase via the blockade of cyclin B1/CDC2 in human ovarian cancer cells.
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硫烷通过人类卵巢癌细胞中的细胞周期蛋白B1/CDC2的阻断在G2/M期诱导细胞周期停滞。
DOI:
10.1186/1757-2215-6-41
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发表时间:
2013-06-26
影响因子:
4
通讯作者:
Hsu YC
中科院分区:
文献类型:
--
作者:
Chang CC;Hung CM;Yang YR;Lee MJ;Hsu YC
Malignant tumors are the single most common cause of death and the mortality rate of ovarian cancer is the highest among gynecological disorders. The excision of benign tumors is generally followed by complete recovery; however, the activity of cancer cells often results in rapid proliferation even after the tumor has been excised completely. Thus, clinical treatment must be supplemented by auxiliary chemotherapy or radiotherapy. Sulforaphane (SFN) is an extract from the mustard family recognized for its anti-oxidation abilities, phase 2 enzyme induction, and anti-tumor activity. This study investigated the cell cycle arrest in G2/M by SFN and the expression of cyclin B1, Cdc2, and the cyclin B1/CDC2 complex in PA-1 cells using western blotting and co-IP western blotting. This study investigated the anticancer effects of dietary isothiocyanate SFN on ovarian cancer, using cancer cells line PA-1. SFN-treated cells accumulated in metaphase by CDC2 down-regulation and dissociation of the cyclin B1/CDC2 complex. Our findings suggest that, in addition to the known effects on cancer prevention, SFN may also provide antitumor activity in established ovarian cancer.
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影响因子:
3.7
作者:
Drews-Elger K;Ortells MC;Rao A;López-Rodriguez C;Aramburu J
通讯作者:
Aramburu J
DOI:
10.1155/2012/415231
发表时间:
2012
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
作者:
Chen MJ;Tang WY;Hsu CW;Tsai YT;Wu JF;Lin CW;Cheng YM;Hsu YC
通讯作者:
Hsu YC
影响因子:
4.1
作者:
Biswas, S.;Hwang, J. W.;Rahman, I.
通讯作者:
Rahman, I.
影响因子:
4.2
作者:
Davis, Rachel;Singh, Karan P.;Shankar, Sharmila
通讯作者:
Shankar, Sharmila
影响因子:
--
作者:
Devi, J. Renuka;Thangam, E. Berla
通讯作者:
Thangam, E. Berla