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NFIC1 inhibits the migration and invasion of MDA-MB-231 cells through S100A2-mediated inactivation of MEK/ERK pathway
被引:0
作者:

Zhang, Jing
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China
Jilin Univ, Sch Life Sci, Changchun 130012, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Wang, Zhaoying
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China
Jilin Univ, Sch Life Sci, Changchun 130012, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Liang, Zehua
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Jin, Chanjuan
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Shi, Yueru
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Fan, Mingyue
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China
Jilin Univ, Sch Life Sci, Changchun 130012, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Hu, Xin
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Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China

Wan, Youzhong
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h-index: 0
机构:
Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China
机构:
[1] Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China
[2] Jilin Univ, Sch Life Sci, Changchun 130012, Jilin, Peoples R China
基金:
中国国家自然科学基金;
关键词:
Triple negative breast cancer;
NFIC1;
MEK;
ERK pathway;
NEGATIVE BREAST-CANCER;
BINDING-PROTEIN S100A2;
TUMOR-SUPPRESSOR GENE;
NUCLEAR FACTOR 1-C2;
OSTEOBLAST DIFFERENTIATION;
PROGNOSTIC-SIGNIFICANCE;
MESENCHYMAL TRANSITION;
CLINICAL-SIGNIFICANCE;
ROOT-FORMATION;
EXPRESSION;
D O I:
10.1016/j.abb.2022.109497
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:
NFIC is a potent transcriptional factor involved in many physiological and pathological processes, including tumorigenesis. However, the role of NFIC1, the longest isoform of NFIC, in the progression of triple negative breast cancer (TNBC) remains elusive. Our study demonstrates that overexpression of NFIC1 inhibits the migration and invasion of TNBC MDA-MB-231 cells. NFIC1 regulates the expression of S100A2, and knockdown of S100A2 reverses the inhibitive effects of NFIC1 on the migration and invasion of MDA-MB-231 cells. Furthermore, knockdown of S100A2 activates the MEK/ERK signaling transduction pathway that is inhibited by NFIC1 overexperssion. Treatment with MEK/ERK pathway inhibitor, U0126, abolishes the effects of S100A2 knockdown. In addition, overexpression of NFIC1 in MDA-MB-231 cells increases the expression of epithelial markers and decreases the expression of mesenchymal markers, and these effects could also be reversed by knockdown of S100A2. Collectively, these results demonstrate that NFIC1 inhibits the Epithelial-mesenchymal transition (EMT) of MDA-MB-231 cells by regulating S100A2 expression, which suppress the activation of MEK/ERK pathway. Therefore, our study confirms the role of NFIC1 as a tumor repressor in TNBC, and reveals the molecular mechanism through which NFIC1 inhibits the migration and invasion of MDA-MB-231 cells.
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JOURNAL OF BIOCHEMISTRY,
2005, 138 (03)
:313-325

Emi, Y
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Univ Hyogo, Grad Sch Life Sci, Harima Sci Park City, Hyogo 6781297, Japan Univ Hyogo, Grad Sch Life Sci, Harima Sci Park City, Hyogo 6781297, Japan

Ueda, K
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Ohnishi, A
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Ikushiro, S
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Iyanagi, T
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Univ Hyogo, Grad Sch Life Sci, Harima Sci Park City, Hyogo 6781297, Japan Univ Hyogo, Grad Sch Life Sci, Harima Sci Park City, Hyogo 6781297, Japan