Estrogen Related Receptors Play Roles in Cancer and Neurodegeneration

By Eric Neeley

Estrogen receptors come in the form of two distinct forms, ER alpha and ER beta. These nuclear receptors are predominantly activated by the hormone 17-beta-estradiol to control transcription of genes throughout the immune, nervous, cardiovascular, and skeletal systems. The classic signaling method of these receptors involves homo- or hetero- receptor dimerization, followed by direct binding to estrogen response elements (ERE). They can also work in concert with other transcription factors, such as SP1 and Fos/Jun, to activate genes which do not contain an ERE. Estrogen receptor over-expression is extremely common in breast cancer, where it is experienced in over 70% of cases.

Anti-estrogens which block ER alpha are the stable clinical therapy for breast cancer, but have side effects and are no longer useful after prolonged treatment where cancers can become resistant. Within this group, when the anti-estrogen drug tamoxifen is used, over 70% of women benefit from its use. Newer treatments that are similar to tamoxifen, such as raloxifene and tormifene, are also common, as well as complete blocking of estrogen signaling with aromatase inihbitors, which block estrogen production. In addition to the role of ERs in morphogenesis, estrogen receptors are widely expressed throughout the brain, where estrogen acts as a trophic factor for neurons. Interestingly, the use of estrogen as a neuroprotective agent against Alzheimer’s disease, Parkinson’s disease, and stroke is currently under investigation. However, the antiapoptotic effects of estrogen in the brain, as well as its ability to downregulate proapoptotic molecules, have been shown in numerous studies.

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