Role of thioredoxin reductase 1 in dysplastic transformation of human breast epithelial cells triggered by chronic oxidative stress.
Role of thioredoxin reductase 1 in dysplastic transformation of human breast epithelial cells triggered by chronic oxidative stress.
复制标题
硫氧还蛋白还原酶1在由慢性氧化应激触发的人乳腺上皮细胞的发育异常转化中的作用。
DOI:
10.1038/srep36860
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发表时间:
2016-11-15
影响因子:
4.6
通讯作者:
Zeng H
中科院分区:
文献类型:
--
作者:
Dong C;Zhang L;Sun R;Liu J;Yin H;Li X;Zheng X;Zeng H
Thioredoxin reductase 1 (TrxR1) is a pivotal intracellular redox sensor and antioxidant enzyme. On the other hand, overexpression of TrxR1 is closely correlated with the initiation of various tumors including breast cancer, though the detailed mechanism remains unclear. Here we investigated the role of TrxR1 in dysplastic transformation of human breast epithelial cell line MCF-10A induced by chronic oxidative stress. Not surprisingly, sustained exposure to H2O2 significantly augmented the expression and activity of TrxR1 in MCF-10A cells. The dysplastically transformed MCF-10A (MCF-10AT) cells undergoing 8-week H2O2 treatment exhibited a certain degree of malignancy in tumorigenicity evaluation. Moreover, TrxR1 inhibitor ethaselen (BBSKE) could partially reverse some malignant phenotypes including epithelial to mesenchymal transition (EMT) of MCF-10AT as well as MCF-7 cells. Collectively, our results supported the considerable involvement of TrxR1 in the onset of breast cancer and BBSKE may be a promising agent against breast cancer.
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影响因子:
50.3
作者:
Cooke VG;LeBleu VS;Keskin D;Khan Z;O'Connell JT;Teng Y;Duncan MB;Xie L;Maeda G;Vong S;Sugimoto H;Rocha RM;Damascena A;Brentani RR;Kalluri R
通讯作者:
Kalluri R
影响因子:
5.8
作者:
Cox, Andrew G.;Brown, Kristin K.;Hampton, Mark B.
通讯作者:
Hampton, Mark B.
影响因子:
--
作者:
Kim, Myung-Chul;Cui, Feng-Ji;Kim, Yongbaek
通讯作者:
Kim, Yongbaek
影响因子:
16.6
作者:
Enroth, Stefan;Johansson, Asa;Enroth, Sofia Bosdotter;Gyllensten, Ulf
通讯作者:
Gyllensten, Ulf
影响因子:
5.6
作者:
Mahalingaiah, Prathap Kumar S.;Ponnusamy, Logeswari;Singh, Kamaleshwar P.
通讯作者:
Singh, Kamaleshwar P.