title: S100A4 participates in epithelial-mesenchymal transition in breast cancer via targeting MMP2.
abstract: Numerous studies have shown that S100A4 acquires its metastasis-promoting effects via inducing epithelial-mesenchymal transition (EMT). However, its role and mechanism in EMT in breast cancer had not been clearly elucidated. Herein, we showed that the knockdown of S100A4 expression in breast cancer cell lines, MDA-MB-231 and MDA-MB-468, inhibited not only cell invasion ability greatly, but also the occurrence of EMT significantly. In addition, S100A4 knockdown could also decrease the expression of MMP2, a promoter and a mediator of the EMT processes in cancer. Above all, restoring the expression of MMP2 in MDA-MB-231 and MDA-MB-468 could not only rescue the invasion ability inhibited by knockdown of S100A4, but also reverse the EMT suppressed by knockdown of S100A4. In summary, our results indicated that S100A4 could promote the invasion ability of breast cancer cells via EMT, more importantly, it could participate in EMT via regulating MMP2 in breast cancer. Therefore, S100A4 could be a candidate biomarker for defining breast cancer metastasis and useful target for therapy.
authors.affiliation: Department of Breast Disease Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China.
authors.forename: Han
authors.initials: H
authors.lastname: Xu
authors.affiliation: Department of Breast Disease Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China.
authors.forename: Mengquan
authors.initials: M
authors.lastname: Li
authors.affiliation: Department of Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Zhou
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China.
authors.forename: Feng
authors.initials: F
authors.lastname: Wang
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China.
authors.forename: Xiangke
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China.
authors.forename: Liuxing
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People's Republic of China. fqx2243@163.com.
authors.forename: Qingxia
authors.initials: Q
authors.lastname: Fan
mesh_terms: D015703:Antigens, CD; D001943:Breast Neoplasms / Q000201:enzymology / Q000473:pathology*; D015820:Cadherins / Q000032:analysis; D045744:Cell Line, Tumor; D058750:Epithelial-Mesenchymal Transition; D005260:Female; D006801:Humans; D020778:Matrix Metalloproteinase 2 / Q000502:physiology*; D009361:Neoplasm Invasiveness; D000071999:S100 Calcium-Binding Protein A4 / Q000502:physiology*; D014746:Vimentin / Q000032:analysis
chemical_list: D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; D000071999:S100 Calcium-Binding Protein A4; D014746:Vimentin; C077591:S100A4 protein, human; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2
keywords: Breast cancer; EMT; MMP2; S100A4