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KMID : 0613820180280020265
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Journal of Life Science
2018 Volume.28 No. 2 p.265 ~ p.273
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Bidirectional Cross-talk Between Estrogen Receptor and Growth Factor Receptors in Breast Cancer Cell
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Min Gye-Sik
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Abstract
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Estrogen (E2) is involved in the development and progression of breast cancer and is mediated by estrogen receptor (ER). ER plays important roles in cellular proliferation, migration, invasion and causing drug resistance through diverse cross-talks with epidermal growth factor receptor (EGFR) and insulin-like growth factor-1 receptor (IGF-1R) signaling pathways in breast cancer cells. Breast cancer is caused mainly by break-down of homeostasis of endocrine signaling pathways especially by the uncontrolled expression and increased activities of E2/IGF-1/EGF, ER/G-protein estrogen receptor (GPER)/ IGF-1R/EGFR and their intracellular signaling mediators. These changes influence the complex cross- talk between E2 and growth factors’ signaling, eventually resulting in the progression of cancer and resistance against endocrine regulators. Thus, elucidation of the molecular mechanisms in stepwise of the cross-talk between E2 and growth factors will contribute to the customized treatment according to the diverse types of breast cancer. In particular, as strategies for the treatment of breast cancer with diverse genotypes and phenotypes, there can be use of aromatase inhibitors and blockers of E2 action for the ER+ hormone-dependent breast cancer cells and use of IGF-1R/EGFR activity blockers for suppression of cancer cell proliferation from the cross-talk between E2 and growth factors. Furthermore, changes in the expression of the ECM molecules regulated by the cross-talk between ER and EGFR/ IGF-1R can be used for the targeted therapeutics against the migration of breast cancer cells. Therefore, it is required for the cross-talk among the signaling pathways of ER, GPER, IGF-1R and EGFR concerning cancer progression to be elucidated in more detail at the molecular level.
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KEYWORD
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Cross-talk, epidermal growth factor receptor (EGFR), estrogen receptor (ER), extracellular matrix molecules (ECM), G-protein estrogen receptor (GPER), insulin-like growth factor receptor (IGFR)
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