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. 2014 Aug 30;7:1525–1533. doi: 10.2147/OTT.S65345

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© 2014 Su et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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ER-α36 and tamoxifen resistance.

Notes: ER-α36 is an important cause of tamoxifen resistance. On the one hand, it activates membrane-initiated signaling pathways, such as MAPK/ERK, PI3K/AKT, and Src/EGFR/STAT5 pathways, causing the agonist effect of tamoxifen. On the other hand, ER-α36 upregulates EGFR and downregulates ER-α66 switching growth status from estrogen-dependent to growth-factor-dependent. Therefore, ER-α36 leads to tamoxifen resistance.

Abbreviations: Akt, protein kinase B; EGFR, epidermal growth factor receptor; ER-α36, estrogen receptor-alpha36; ER-α66, estrogen receptor-alpha66; ERK, extracellular signal-regulated kinase; MAPK, mitogen-activated protein kinases; MCF-7/TAM, tamoxifen-resistant MCF-7 cell line; PI3K, phosphatidylinositide 3-kinase; STAT5, signal transducer and activator of transcription 5.