Estrogen therapy may still hold the key to fight specific ER resistant breast cancers

Estrogen receptors (ERs) may act as a hub where several molecular pathways converge, while the transcriptional activity of ERs drives all cellular functions. ER regulated genes initiate, complete and supervise the replication and recombination of DNA. There is a unique upregulative feedback mechanism between estrogens and ERs. Both high and low estrogen levels promote an increased expression and transcriptional activity of ERs so as to restore or augment cellular ER signaling. In turn, both low and high ER expressions induce powerful estrogen synthesis for the improvement or augmentation of crucial ER signaling. Estrogens induce a balanced activation of estrogen liganded and non liganded growth factor receptor (GFR) mediated transactivation functions of ERs providing immense reserve capacities in emergency conditions. When liganded ER signaling is endangered by either estrogen deficiency or ER resistance, a strong compensatory upregulation of non liganded ER activation may save the surveillance of genomic machinery. Increased estrogen concentrations amplify both ER expression and estrogen synthesis strongly upregulating the ER signaling and genomic stabilization. The DNA protective effect of high estrogen concentrations improves all physiologic functions of healthy cells, while suppressing the survival possibility of cancer cells in a Janus-faced manner.

Experimental studies reveal a strong interplay


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