The Molecular Mechanism of Epithelial-Mesenchymal Transition for Breast Carcinogenesis

被引:23
作者
Li, Chia-Jung [1 ,2 ]
Chu, Pei-Yi [3 ,4 ,5 ]
Yiang, Giou-Teng [6 ,7 ]
Wu, Meng-Yu [6 ,7 ]
机构
[1] Kaohsiung Vet Gen Hosp, Dept Obstet & Gynecol, Kaohsiung 813, Taiwan
[2] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung 804, Taiwan
[3] Fu Jen Catholic Univ, Coll Med, Sch Med, New Taipei 242, Taiwan
[4] Show Chwan Mem Hosp, Dept Pathol, Changhua 500, Taiwan
[5] Chung Chou Univ Sci & Technol, Dept Hlth Food, Changhua 510, Taiwan
[6] Taipei Tzu Chi Hosp, Buddhist Tzu Chi Med Fdn, Dept Emergency Med, New Taipei 231, Taiwan
[7] Tzu Chi Univ, Sch Med, Dept Emergency Med, Hualien 970, Taiwan
关键词
breast cancer; transforming growth factor-beta; epithelial-to-mesenchymal transition; signaling pathway; NF-KAPPA-B; MATRIX METALLOPROTEINASES; TUMOR MICROENVIRONMENT; CONFERS RESISTANCE; BETA-CATENIN; CANCER CELLS; EXPRESSION; EMT; METASTASIS; GROWTH;
D O I
10.3390/biom9090476
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
The transforming growth factor-beta (TGF-beta) signaling pathway plays multiple regulatory roles in the tumorigenesis and development of cancer. TGF-beta can inhibit the growth and proliferation of epithelial cells and induce apoptosis, thereby playing a role in inhibiting breast cancer. Therefore, the loss of response in epithelial cells that leads to the inhibition of cell proliferation due to TGF-beta is a landmark event in tumorigenesis. As tumors progress, TGF-beta can promote tumor cell invasion, metastasis, and drug resistance. At present, the above-mentioned role of TGF-beta is related to the interaction of multiple signaling pathways in the cell, which can attenuate or abolish the inhibition of proliferation and apoptosis-promoting effects of TGF-beta and enhance its promotion of tumor progression. This article focuses on the molecular mechanisms through which TGF-beta interacts with multiple intracellular signaling pathways in tumor progression and the effects of these interactions on tumorigenesis.
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页数:14
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