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To understand the potential effects of cancer cells on surrounding normal mammary epithelial cells, we performed direct co-culture of non-tumorigenic mammary epithelial MCF10A cells and various breast cancer cells. Firstly, we observed dynamic cell-cell interactions between the MCF10A cells and breast cancer cells including lamellipodia or nanotube-like contacts and transfer of extracellular vesicles. Co-cultured MCF10A cells exhibited features of epithelial-mesenchymal transition, and showed increased capacity of cell proliferation, migration, colony formation, and 3-dimensional sphere formation. Direct co-culture showed most distinct phenotype changes in MCF10A cells followed by conditioned media treatment and indirect co-culture. Transcriptome analysis and phosphor-protein array suggested that several cancer-related pathways are significantly dysregulated in MCF10A cells after the direct co-culture with breast cancer cells. S100A8 and S100A9 showed distinct up-regulation in the co-cultured MCF10A cells and their microenvironmental upregulation was also observed in the orthotropic xenograft of syngeneic mouse mammary tumors. When S100A8/A9 overexpression was induced in MCF10A cells, the cells showed phenotypic features of directly co-cultured MCF10A cells in terms of in vitro cell behaviors and signaling activities suggesting a S100A8/A9-mediated transition program in non-tumorigenic epithelial cells. This study suggests the possibility of dynamic cell-cell interactions between non-tumorigenic mammary epithelial cells and breast cancer cells that could lead to a substantial transition in molecular and functional characteristics of mammary epithelial cells.

Titel:	S100A8/A9 mediate the reprograming of normal mammary epithelial cells induced by dynamic cell-cell interactions with adjacent breast cancer cells.
Autor/in / Beteiligte Person:	Jo, SH ; Heo, WH ; Son, HY ; Quan, M ; Hong, BS ; Kim, JH ; Lee, HB ; Han, W ; Park, Y ; Lee, DS ; Kwon, NH ; Park, MC ; Chae, J ; Kim, JI ; Noh, DY ; Moon, HG
Link:	Full Text Finder (Volltext)
Zeitschrift:	Scientific reports, Jg. 11 (2021-01-14), Heft 1, S. 1337
Veröffentlichung:	London : Nature Publishing Group, copyright 2011-, 2021
Medientyp:	academicJournal
ISSN:	2045-2322 (electronic)
DOI:	10.1038/s41598-020-80625-2
Schlagwort:	Animals Breast Neoplasms pathology Cell Line, Tumor Epithelial Cells pathology Female Humans Mammary Glands, Human pathology Mice Mice, Inbred BALB C Breast Neoplasms metabolism Calgranulin A metabolism Calgranulin B metabolism Cell Communication Epithelial Cells metabolism Mammary Glands, Human metabolism Neoplasm Proteins metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [Sci Rep] 2021 Jan 14; Vol. 11 (1), pp. 1337. <i>Date of Electronic Publication: </i>2021 Jan 14. MeSH Terms: Cell Communication* ; Breast Neoplasms / metabolism ; Calgranulin A / metabolism ; Calgranulin B / metabolism ; Epithelial Cells / metabolism ; Mammary Glands, Human / metabolism ; Neoplasm Proteins / metabolism ; Animals ; Breast Neoplasms / pathology ; Cell Line, Tumor ; Epithelial Cells / pathology ; Female ; Humans ; Mammary Glands, Human / pathology ; Mice ; Mice, Inbred BALB C References: Joyce, J. A. & Pollard, J. W. Microenvironmental regulation of metastasis. Nat. Rev. Cancer 9, 239–252. https://doi.org/10.1038/nrc2618 (2009). (PMID: 10.1038/nrc261819279573) ; Hanahan, D. & Coussens, L. M. Accessories to the crime: Functions of cells recruited to the tumor microenvironment. Cancer Cell 21, 309–322. https://doi.org/10.1016/j.ccr.2012.02.022 (2012). (PMID: 10.1016/j.ccr.2012.02.02222439926) ; Place, A. E., Jin Huh, S. & Polyak, K. The microenvironment in breast cancer progression: biology and implications for treatment. Breast Cancer Res. 13, 227. https://doi.org/10.1186/bcr2912 (2011). (PMID: 10.1186/bcr2912220780263326543) ; Gajewski, T. F., Schreiber, H. & Fu, Y. X. Innate and adaptive immune cells in the tumor microenvironment. Nat. Immunol. 14, 1014–1022. https://doi.org/10.1038/ni.2703 (2013). (PMID: 10.1038/ni.2703240481234118725) ; Kalluri, R. The biology and function of fibroblasts in cancer. Nat. Rev. Cancer 16, 582–598. https://doi.org/10.1038/nrc.2016.73 (2016). (PMID: 10.1038/nrc.2016.7327550820) ; Lee, J. et al. Transition into inflammatory cancer-associated adipocytes in breast cancer microenvironment requires microRNA regulatory mechanism. PLoS ONE 12, e0174126. https://doi.org/10.1371/journal.pone.0174126 (2017). (PMID: 10.1371/journal.pone.0174126283339775363867) ; Pardoll, D. M. The blockade of immune checkpoints in cancer immunotherapy. Nat. Rev. Cancer 12, 252–264. https://doi.org/10.1038/nrc3239 (2012). (PMID: 10.1038/nrc3239224378704856023) ; Klemm, F. & Joyce, J. A. Microenvironmental regulation of therapeutic response in cancer. Trends Cell Biol. 25, 198–213. https://doi.org/10.1016/j.tcb.2014.11.006 (2015). (PMID: 10.1016/j.tcb.2014.11.00625540894) ; Fang, H. & Declerck, Y. A. Targeting the tumor microenvironment: from understanding pathways to effective clinical trials. Cancer Res. 73, 4965–4977. https://doi.org/10.1158/0008-5472.CAN-13-0661 (2013). (PMID: 10.1158/0008-5472.CAN-13-066123913938) ; Porazinski, S. et al. EphA2 drives the segregation of Ras-transformed epithelial cells from normal neighbors. Curr. Biol. 26, 3220–3229. https://doi.org/10.1016/j.cub.2016.09.037 (2016). (PMID: 10.1016/j.cub.2016.09.03727839970) ; Saitoh, S. et al. Rab5-regulated endocytosis plays a crucial role in apical extrusion of transformed cells. Proc. Natl. Acad. Sci. USA 114, E2327–E2336. https://doi.org/10.1073/pnas.1602349114 (2017). (PMID: 10.1073/pnas.1602349114282706085373379) ; Hogan, C. et al. Characterization of the interface between normal and transformed epithelial cells. Nat. Cell Biol. 11, 460–467. https://doi.org/10.1038/ncb1853 (2009). (PMID: 10.1038/ncb185319287376) ; Gudjonsson, T. et al. Normal and tumor-derived myoepithelial cells differ in their ability to interact with luminal breast epithelial cells for polarity and basement membrane deposition. J. Cell Sci. 115, 39–50 (2002). (PMID: 10.1242/jcs.115.1.39) ; Allinen, M. et al. Molecular characterization of the tumor microenvironment in breast cancer. Cancer Cell 6, 17–32. https://doi.org/10.1016/j.ccr.2004.06.010 (2004). (PMID: 10.1016/j.ccr.2004.06.01015261139) ; Mattila, P. K. & Lappalainen, P. Filopodia: Molecular architecture and cellular functions. Nat. Rev. Mol. Cell Biol. 9, 446–454. https://doi.org/10.1038/nrm2406 (2008). (PMID: 10.1038/nrm240618464790) ; Rustom, A., Saffrich, R., Markovic, I., Walther, P. & Gerdes, H. H. Nanotubular highways for intercellular organelle transport. Science 303, 1007–1010. https://doi.org/10.1126/science.1093133 (2004). (PMID: 10.1126/science.109313314963329) ; Mani, S. A. et al. The epithelial-mesenchymal transition generates cells with properties of stem cells. Cell 133, 704–715 (2008). (PMID: 10.1016/j.cell.2008.03.027) ; Finak, G. et al. Stromal gene expression predicts clinical outcome in breast cancer. Nat. Med. 14, 518–527. https://doi.org/10.1038/nm1764 (2008). (PMID: 10.1038/nm176418438415) ; Kajita, M. et al. Interaction with surrounding normal epithelial cells influences signalling pathways and behaviour of Src-transformed cells. J. Cell Sci. 123, 171–180. https://doi.org/10.1242/jcs.057976 (2010). (PMID: 10.1242/jcs.05797620026643) ; Ivers, L. P. et al. Dynamic and influential interaction of cancer cells with normal epithelial cells in 3D culture. Cancer Cell Int. 14, 108. https://doi.org/10.1186/s12935-014-0108-6 (2014). (PMID: 10.1186/s12935-014-0108-6253790144221723) ; Trujillo, K. A. et al. Markers of fibrosis and epithelial to mesenchymal transition demonstrate field cancerization in histologically normal tissue adjacent to breast tumors. Int. J. Cancer 129, 1310–1321. https://doi.org/10.1002/ijc.25788 (2011). (PMID: 10.1002/ijc.25788211050473249233) ; Fong, E. L. et al. A 3D in vitro model of patient-derived prostate cancer xenograft for controlled interrogation of in vivo tumor-stromal interactions. Biomaterials 77, 164–172. https://doi.org/10.1016/j.biomaterials.2015.10.059 (2016). (PMID: 10.1016/j.biomaterials.2015.10.05926599623) ; Roh-Johnson, M. et al. Macrophage-dependent cytoplasmic transfer during melanoma invasion in vivo. Dev. Cell 43, 549–562. https://doi.org/10.1016/j.devcel.2017.11.003 (2017). (PMID: 10.1016/j.devcel.2017.11.003292072585728704) ; Leung, C. T. & Brugge, J. S. Outgrowth of single oncogene-expressing cells from suppressive epithelial environments. Nature 482, 410–413. https://doi.org/10.1038/nature10826 (2012). (PMID: 10.1038/nature10826223185153297969) ; Kajita, M. & Fujita, Y. EDAC: Epithelial defence against cancer-cell competition between normal and transformed epithelial cells in mammals. J. Biochem. 158, 15–23. https://doi.org/10.1093/jb/mvv050 (2015). (PMID: 10.1093/jb/mvv05025991731) ; Srikrishna, G. S100A8 and S100A9: new insights into their roles in malignancy. J. Innate Immun. 4, 31–40. https://doi.org/10.1159/000330095 (2012). (PMID: 10.1159/00033009521912088) ; Moon, A. et al. Global gene expression profiling unveils S100A8/A9 as candidate markers in H-ras-mediated human breast epithelial cell invasion. Mol. Cancer Res. 6, 1544–1553. https://doi.org/10.1158/1541-7786.MCR-08-0189 (2008). (PMID: 10.1158/1541-7786.MCR-08-018918922970) ; Yong, H. Y. et al. Identification of H-Ras-specific motif for the activation of invasive signaling program in human breast epithelial cells. Neoplasia 13, 98–107 (2011). (PMID: 10.1593/neo.101088) ; Wiza, C., Nascimento, E. B. & Ouwens, D. M. Role of PRAS40 in Akt and mTOR signaling in health and disease. Am. J. Physiol. Endocrinol. Metab. 302, E1453-1460. https://doi.org/10.1152/ajpendo.00660.2011 (2012). (PMID: 10.1152/ajpendo.00660.201122354785) ; Kim, L. C., Cook, R. S. & Chen, J. mTORC1 and mTORC2 in cancer and the tumor microenvironment. Oncogene 36, 2191–2201. https://doi.org/10.1038/onc.2016.363 (2017). (PMID: 10.1038/onc.2016.36327748764) ; Duluc, C. et al. Pharmacological targeting of the protein synthesis mTOR/4E-BP1 pathway in cancer-associated fibroblasts abrogates pancreatic tumour chemoresistance. EMBO Mol. Med. 7, 735–753. https://doi.org/10.15252/emmm.201404346 (2015). (PMID: 10.15252/emmm.201404346258341454459815) Grant Information: NRF-2019R1C1C1006898 National Research Foundation of Korea; NRF-2019R1A2C2005277 National Research Foundation of Korea; HA15C0011 Korea Health Industry Development Institute Substance Nomenclature: 0 (Calgranulin A) ; 0 (Calgranulin B) ; 0 (Neoplasm Proteins) ; 0 (S100A8 protein, human) ; 0 (S100A9 protein, human) Entry Date(s): Date Created: 20210115 Date Completed: 20210810 Latest Revision: 20210930 Update Code: 20231215 PubMed Central ID: PMC7809201

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S100A8/A9 mediate the reprograming of normal mammary epithelial cells induced by dynamic cell-cell interactions with adjacent breast cancer cells.