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Newcastle disease virus (NDV) is endowed with the oncolytic ability to kill tumor cells, while rarely causing side effects in normal cells. Both estrogen receptor α (ERα) and the G protein estrogen receptor (GPER) modulate multiple biological activities in response to estrogen, including apoptosis in breast cancer (BC) cells. Here, we investigated whether NDV-D90, a novel strain isolated from natural sources in China, promoted apoptosis by modulating the expression of ERα or the GPER in BC cells exposed to 17β-estradiol (E2). We found that NDV-D90 significantly killed the tumor cell lines MCF-7 and BT549 in a time- and dose-dependent manner. We also found that NDV-D90 exerted its effects on the two cell lines mainly by inducing apoptosis but not necrosis. NDV-D90 induced apoptosis via the intrinsic and extrinsic signaling pathways in MCF-7 cells (ER-positive cells) during E2 exposure not only by disrupting the E2/ERα axis and enhancing GPER expression but also by modulating the expression of several apoptosis-related proteins through ERα-and GPER-independent processes. NDV-D90 promoted apoptosis via the intrinsic signaling pathway in BT549 cells (ER-negative cells), possibly by impairing E2-mediated GPER expression. Furthermore, NDV-D90 exerted its antitumor effects in vivo by inducing apoptosis. Overall, these results demonstrated that NDV-D90 promotes apoptosis by differentially modulating the expression of ERα and the GPER in ER-positive and negative BC cells exposed to estrogen, respectively, and can be utilized as an effective approach to treating BC.

Titel:	NDV-D90 inhibits 17β-estradiol-mediated resistance to apoptosis by differentially modulating classic and nonclassic estrogen receptors in breast cancer cells.
Autor/in / Beteiligte Person:	Shan, P ; Tang, B ; Xie, S ; Zhang, Z ; Fan, J ; Wei, Z ; Song, C
Link:	Full Text Finder (Volltext)
Zeitschrift:	Journal of cellular biochemistry, Jg. 122 (2021), Heft 1, S. 3-15
Veröffentlichung:	<2004>- : Hoboken, NJ : Wiley-Liss ; <i>Original Publication</i>: New York : Liss, c1982-, 2021
Medientyp:	academicJournal
ISSN:	1097-4644 (electronic)
DOI:	10.1002/jcb.28118
Schlagwort:	Animals Breast Neoplasms metabolism Breast Neoplasms therapy Cell Proliferation Estrogens pharmacology Female Humans Mice Mice, Nude Receptors, Estrogen genetics Tumor Cells, Cultured Xenograft Model Antitumor Assays Apoptosis Breast Neoplasms pathology Estradiol pharmacology Gene Expression Regulation, Neoplastic Newcastle disease virus growth & development Oncolytic Virotherapy methods Receptors, Estrogen metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [J Cell Biochem] 2021 Jan; Vol. 122 (1), pp. 3-15. <i>Date of Electronic Publication: </i>2020 Sep 28. MeSH Terms: Apoptosis* ; Gene Expression Regulation, Neoplastic* ; Breast Neoplasms / pathology ; Estradiol / pharmacology ; Newcastle disease virus / growth & development ; Oncolytic Virotherapy / methods ; Receptors, Estrogen / *metabolism ; Animals ; Breast Neoplasms / metabolism ; Breast Neoplasms / therapy ; Cell Proliferation ; Estrogens / pharmacology ; Female ; Humans ; Mice ; Mice, Nude ; Receptors, Estrogen / genetics ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays References: International Agency for Research on Cancer (2013). International Agency for Research on Cancer. Available at: http://www.iarc.fr/en/media-centre/pr/2013/pdfs/pr223_E.pdf (accessed December 12, 2013). ; Evans RM. 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Contributed Indexing: Keywords: G protein estrogen receptor (GPER); Newcastle disease virus-D90 (NDV-D90); apoptosis; breast cancer (BC); estrogen receptor-alpha Substance Nomenclature: 0 (Estrogens) ; 0 (Receptors, Estrogen) ; 4TI98Z838E (Estradiol) Entry Date(s): Date Created: 20200928 Date Completed: 20210727 Latest Revision: 20210727 Update Code: 20231215

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NDV-D90 inhibits 17β-estradiol-mediated resistance to apoptosis by differentially modulating classic and nonclassic estrogen receptors in breast cancer cells.