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Triolein from Coix lacryma-jobi induces cell cycle arrest through p53/p21 signaling pathway

Hien Tran, Thi LU ; Ha, Do Thi; Truong, Do Minh; Duc, Loi Vu; Dao, Trong Tuan; Binh, Bui Thi and Hai, Nguyen Thanh (2016) In Biomedical and Pharmacology Journal 9(2). p.519-524
Abstract

p53, a tumor suppressor protein, has important roles in DNA repair, cell cycle and apoptosis, is a one of the key events in cancer development. Coix lacryma-jobi seed has been used as a food and traditional medicine plant with anti-oxidant, anti-cancer and anti-diabetic effects. In currently research, we identified the most potent p53-increasing compound among 4 compounds (1-4) found in Coix lacryma-jobi and demonstrated its molecular mechanism in MCF-7 cells. Among the four isolated compounds (1-4), triolein most increased p53. Triolein treatment induced p53, p21, p27 and Bax in MCF-7 cells. Moreover, triolein caused S phase arrest through suppression of CDK1, phopho-Rb and E2F1 in dose-dependent manner. We also observed the decreasing... (More)

p53, a tumor suppressor protein, has important roles in DNA repair, cell cycle and apoptosis, is a one of the key events in cancer development. Coix lacryma-jobi seed has been used as a food and traditional medicine plant with anti-oxidant, anti-cancer and anti-diabetic effects. In currently research, we identified the most potent p53-increasing compound among 4 compounds (1-4) found in Coix lacryma-jobi and demonstrated its molecular mechanism in MCF-7 cells. Among the four isolated compounds (1-4), triolein most increased p53. Triolein treatment induced p53, p21, p27 and Bax in MCF-7 cells. Moreover, triolein caused S phase arrest through suppression of CDK1, phopho-Rb and E2F1 in dose-dependent manner. We also observed the decreasing of DNA synthesis by triolein. These data suggest that triolein may induced cell cycle restart involve DNA synthesis and apoptosis pathway in MCF-7 cells.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Apoptosis, Coix lacryma-jobi, DNA synthesis, MCF-7 cells, Triolein
in
Biomedical and Pharmacology Journal
volume
9
issue
2
pages
6 pages
publisher
Oriental Scientific Publishing Company
external identifiers
  • scopus:85009403504
ISSN
0974-6242
DOI
10.13005/bpj/967
language
English
LU publication?
yes
id
8573a1d9-9672-4336-a183-50a05fb95e0e
date added to LUP
2017-02-21 10:33:43
date last changed
2017-02-21 10:33:43
@article{8573a1d9-9672-4336-a183-50a05fb95e0e,
  abstract     = {<p>p53, a tumor suppressor protein, has important roles in DNA repair, cell cycle and apoptosis, is a one of the key events in cancer development. Coix lacryma-jobi seed has been used as a food and traditional medicine plant with anti-oxidant, anti-cancer and anti-diabetic effects. In currently research, we identified the most potent p53-increasing compound among 4 compounds (1-4) found in Coix lacryma-jobi and demonstrated its molecular mechanism in MCF-7 cells. Among the four isolated compounds (1-4), triolein most increased p53. Triolein treatment induced p53, p21, p27 and Bax in MCF-7 cells. Moreover, triolein caused S phase arrest through suppression of CDK1, phopho-Rb and E2F1 in dose-dependent manner. We also observed the decreasing of DNA synthesis by triolein. These data suggest that triolein may induced cell cycle restart involve DNA synthesis and apoptosis pathway in MCF-7 cells.</p>},
  author       = {Hien Tran, Thi and Ha, Do Thi and Truong, Do Minh and Duc, Loi Vu and Dao, Trong Tuan and Binh, Bui Thi and Hai, Nguyen Thanh},
  issn         = {0974-6242},
  keyword      = {Apoptosis,Coix lacryma-jobi,DNA synthesis,MCF-7 cells,Triolein},
  language     = {eng},
  number       = {2},
  pages        = {519--524},
  publisher    = {Oriental Scientific Publishing Company},
  series       = {Biomedical and Pharmacology Journal},
  title        = {Triolein from Coix lacryma-jobi induces cell cycle arrest through p53/p21 signaling pathway},
  url          = {http://dx.doi.org/10.13005/bpj/967},
  volume       = {9},
  year         = {2016},
}