1. Correction to: Calycosin inhibits the in vitro and in vivo growth of breast cancer cells through WDR7-7-GPR30 Signaling
- Author
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Qianyao Ren, Jing Tian, Yong Wang, Jian Chen, Xing Zhang, Yue Huang, Huiling Lu, and Rong Li
- Subjects
0301 basic medicine ,Cancer Research ,GPR30 ,Breast Neoplasms ,lcsh:RC254-282 ,Receptors, G-Protein-Coupled ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Breast cancer ,In vivo ,WDR7-7 ,Cell Line, Tumor ,Medicine ,Animals ,Humans ,skin and connective tissue diseases ,Cell Proliferation ,business.industry ,Research ,Correction ,Calycosin ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Antineoplastic Agents, Phytogenic ,Isoflavones ,Xenograft Model Antitumor Assays ,In vitro ,Up-Regulation ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Oncology ,chemistry ,Receptors, Estrogen ,Apoptosis ,030220 oncology & carcinogenesis ,Long non-coding RNA ,Cancer research ,MCF-7 Cells ,Female ,RNA, Long Noncoding ,Breast cancer cells ,business ,GPER ,Signal Transduction - Abstract
Background Clinically, breast cancer is generally classified into estrogen receptor-positive (ER+) or estrogen receptor-negative (ER−) subtypes. The phytoestrogen calycosin has been shown to inhibit the proliferation of ER+ cells, which may be mediated by a feedback loop that involves miR-375, RAS dexamethasone-induced 1 (RASD1), and ERα. However, how calycosin acts on ER− breast cancer cells remains unclear. Results Here, we show that calycosin inhibited the proliferation of both ER− (MDA-MB-468 and SKBR3) and ER+ breast cancer cells (MCF-7 and T47D) and that these inhibitory effects were associated with the up-regulation of the long non-coding RNA (lncRNA) WDR7-7. For the first time, we demonstrate that the expression of WDR7-7 is reduced in breast cancer cell lines and that the overexpression of WDR7-7 inhibits growth through a mechanism that involves G-protein coupled estrogen receptor 30 (GPR30). Meanwhile, we show that calycosin stimulated the WDR7-7-GPR30 signaling pathway in MCF-7, T47D, MDA-MB-468, and SKBR3 breast cancer cells. In contrast, in MCF10A and GPR30-deficient MDA-MB-231 cells, due to a lack of WDR7-7-GPR30 for activation, calycosin failed to inhibit cell growth. Additionally, in all four GPR30-positive breast cancer lines, calycosin decreased the phosphorylation levels of SRC, EGFR, ERK1/2 and Akt, but the inhibition of WDR7-7 blocked these changes and increased proliferation. In mice bearing MCF-7 or SKBR3 xenografts, tumor growth was inhibited by calycosin, and changes in expression the levels of WDR7-7 and GPR30 in tumor tissues were similar to those in cultured MCF-7 and SKBR3 cells. Conclusions These results suggest the possibility that calycosin inhibited the proliferation of breast cancer cells, at least partially, through WDR7-7-GPR30 signaling, which may explain why calycosin can exert inhibitory effects on ER− breast cancer. Electronic supplementary material The online version of this article (10.1186/s13046-017-0625-y) contains supplementary material, which is available to authorized users.
- Published
- 2017