title: SMC1 promotes epithelial-mesenchymal transition in triple-negative breast cancer through upregulating Brachyury.
abstract: Triple-negative breast cancer (TNBC) is a special subtype of breast cancer, which is characterized by the negative form of estrogen receptor (ER), progesterone receptor (PR) and human epithelial growth factor receptor 2 (HER2). TNBC accounts for ~15% of all breast cancer forms, and often leads to high mortality and poor prognosis. Structural maintenance of chromosome 1 (SMC1) is a subunit of the cohesion protein complex. Brachyury is a protein that is encoded by the T gene in humans, which is a transcription factor within the T-box complex of genes. Epithelial-mesenchymal transition (EMT) is a ubiquitous process in the body, and in particular, induces metastasis and the proliferation of cancer cells. In the present study, we found that SMC1 expression in TNBC tissues exceeded its expression in adjacent non-tumor tissues. Similarly, the expression of SMC1 in TNBC cell lines (hs578T and HCC1937) was found to be higher than in MCF10a and MCF7 cells. Subsequently, SMC1 was overexpressed and silenced in hs578T and HCC1937 cells through plasmid and siRNA transfection, respectively. The results showed that the high expression of SMC1 often promoted EMT, accompanied by the enhanced expression of Brachyury. Besides, upregulated expression of Brachyury through plasmid transfection also significantly improved the level of EMT, which further indicated that SMC1 increased EMT in TNBC through the induction of Brachyury expression. Taken together, these results contributed to a better understanding of the pathogenesis of TNBC, which also provided an experimental basis for the prevention, diagnosis and treatment of TNBC.
authors.affiliation: Department of Oncology, Changhai Hospital Affiliated to The Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Kaichun
authors.initials: K
authors.lastname: Li
authors.affiliation: Department of Oncology, Changhai Hospital Affiliated to The Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Mingzhen
authors.initials: M
authors.lastname: Ying
authors.affiliation: Department of Oncology, Changhai Hospital Affiliated to The Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Dan
authors.initials: D
authors.lastname: Feng
authors.affiliation: Department of Pathology, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, P.R. China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Oncology, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, P.R. China.
authors.forename: Jingwen
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Oncology, Changhai Hospital Affiliated to The Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Yajie
authors.initials: Y
authors.lastname: Wang
mesh_terms: D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism*; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D002868:Chromosomal Proteins, Non-Histone / Q000235:genetics* / Q000378:metabolism*; D058750:Epithelial-Mesenchymal Transition; D005260:Female; D005326:Fetal Proteins / Q000378:metabolism*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D061986:MCF-7 Cells; D020825:T-Box Domain Proteins / Q000378:metabolism*; D064726:Triple Negative Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D015854:Up-Regulation; D000098908:Brachyury Protein; D000098550:Structural Maintenance of Chromosome Protein 1
chemical_list: D018797:Cell Cycle Proteins; D002868:Chromosomal Proteins, Non-Histone; D005326:Fetal Proteins; D020825:T-Box Domain Proteins; D000098908:Brachyury Protein; D000098550:Structural Maintenance of Chromosome Protein 1