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The Role of MRE11 in the IL-6/STAT3 Pathway of Lung Cancer Cells
被引:0
|作者:
Wu, Ching-Yuan
[1
,2
,3
]
Shu, Li-Hsin
[1
]
Liu, Hung-Te
[1
]
Cheng, Yu-Ching
[1
]
Wu, Yu-Huei
[4
]
Wu, Yu-Heng
[5
]
机构:
[1] Chiayi Chang Gung Mem Hosp, Dept Chinese Med, Chiayi 613, Taiwan
[2] Chang Gung Univ, Coll Med, Sch Chinese Med, Taoyuan 333, Taiwan
[3] Chang Gung Univ Sci & Technol, Coll Human Ecol, Res Ctr Chinese Herbal Med, Taoyuan 333, Taiwan
[4] Chang Gung Univ, Dept Biomed Sci, Taoyuan 333, Taiwan
[5] Natl Sun Yat Sen Univ, Dept Elect Engn, Kaohsiung 804, Taiwan
关键词:
MRE11;
lung cancer;
STAT3;
IL-6;
macrophage;
ACTIVATING-FACTOR;
STAT3;
MACROPHAGE;
DNA;
INTERLEUKIN-6;
PURIFICATION;
RECRUITMENT;
INVASION;
GROWTH;
IL-6;
D O I:
10.3390/cimb44120418
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
MRE11 is a pivotal protein for ATM activation during double-strand DNA break. ATM kinase activations may act as lung cancer biomarkers. The IL-6/STAT3 pathway plays an important role in tumor metastasis, including lung cancer. However, the mechanism between MRE11 and the IL-6/STAT3 pathway is still unclear. In this study, we discovered that MRE11 can interact with STAT3 under IL-6 treatment and regulate STAT3 Tyr705 phosphorylation. After the knockdown of MRE11 in lung cancer cells, we discovered that IL-6 or the conditional medium of THP-1 cells can induce the mRNA expression of STAT3 downstream genes, including CCL2, in the control cells, but not in MRE11-knockdown lung cancer cells. Moreover, CCL2 secretion was lower in MRE11-knockdown lung cancer cells than in control cells after treatment with the conditional medium of RAW264.7 cells. In addition, MRE11 deficiency in lung cancer cells decreases their ability to recruit RAW 264.7 cells. Furthermore, MRE11 is a potential target for lung cancer therapy.
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页码:6132 / 6144
页数:13
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