title: Effect of truncated neurokinin-1 receptor expression changes on the interaction between human breast cancer and bone marrow-derived mesenchymal stem cells.
abstract: Previous studies in breast cancer cell lines showed that truncated neurokinin receptor-1 (NK1R-Tr) was able to promote malignant transformation of breast cells, and NK1R-Tr may contribute to tumor progression and promote distant metastasis in human breast cancer. A co-culture model of breast cancer and bone marrow-derived human mesenchymal stem (HMSC-bm) cells showed that HMSC-bm inhibited the growth of breast cancer cells and entered the bone marrow at early stages. Down-regulation of NK1R-Tr may be a key factor in maintaining the quiescent phenotype of breast cancer cells among bone marrow stroma. Stromal-derived factor (SDF)-1α expression was negatively correlated with NK1R-Tr expression in breast cancer cells. Secretion of SDF-1α by HMSC-bm may maintain the quiescent phenotype of breast cancer cells among bone marrow stroma by down-regulating NK1R-Tr expression. Transforming growth factor (TGF)-β1 expression was positively associated with NK1R-Tr expression in breast cancer cells. In a co-culture system, MDA-MB-231-TGF-β1I (TGF-β genes were suppressed using specific shRNA) cells were able to attach to HMSC-bm quickly, indicating that TGF-β1 was also a key factor for maintaining the quiescent phenotype of breast cancer cells in bone marrow stroma. However, the detailed mechanism still remained unclear and could involve other molecules, in addition to NK1R-Tr.
authors.affiliation: Department of Clinical Laboratory, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin, 300060, China; Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin, 300060, China.
authors.forename: Yunli
authors.initials: Y
authors.lastname: Zhou
authors.forename: Duo
authors.initials: D
authors.lastname: Zuo
authors.forename: Meng
authors.initials: M
authors.lastname: Wang
authors.forename: Yongci
authors.initials: Y
authors.lastname: Zhang
authors.forename: Man
authors.initials: M
authors.lastname: Yu
authors.forename: Jie
authors.initials: J
authors.lastname: Yang
authors.forename: Zhi
authors.initials: Z
authors.lastname: Yao
mesh_terms: D001854:Bone Marrow Cells / Q000378:metabolism*; D019046:Bone Marrow Neoplasms / Q000556:secondary; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D002450:Cell Communication; D002460:Cell Line; D049109:Cell Proliferation; D054377:Chemokine CXCL12 / Q000235:genetics / Q000378:metabolism; D018920:Coculture Techniques; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000378:metabolism* / Q000473:pathology; D018040:Receptors, Neurokinin-1 / Q000235:genetics / Q000378:metabolism*; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D054377:Chemokine CXCL12; D018040:Receptors, Neurokinin-1; D011994:Recombinant Proteins; D053773:Transforming Growth Factor beta1