Estrogen Receptors as Key Factors in Carcinogenesis

Despite continuous advances in the development of methodologies for the diagnosis and therapeutic treatment of cancer, the disease remains a primary cause of mortality worldwide. A comprehensive understanding of the molecular mechanisms underlying cancer could ultimately lead to increasingly effective therapeutic interventions. One approach that could be adopted is to formulate methodologies that impede cell signalling and/or the expression of genes pivotal to carcinogenesis. A notable example of this strategy is the focus on the estrogen receptor, a key player in the development of various types of cancer. The deregulation of this receptor, and the subsequent impact on cell function, is a critical factor in the progression of these diseases. This renders it a significant therapeutic target. Furthermore, the microenvironment has been demonstrated to exert a significant influence on the development of cancers. A mounting body of evidence indicates that the abnormal physical properties of the tumour microenvironment can induce widespread changes, leading to the selection of characteristic tumour cell abilities and subsequent clonal proliferation. This process is accompanied by an increased capacity for invasive growth and, notably, the induction of multidrug resistance. The present article focuses on presenting the structure and role of the estrogen receptor in selected hormone-dependent cancers, its involvement in the formation of the tumor microenvironment, currently used therapeutic methods in the treatment of these cancers, and the challenges associated with them. Each new discovery in the field of cancer biology offers the prospect of developing new potential treatments, including targeted therapies aimed at improving the survival of patients suffering from hormone-dependent malignant tumours. Although the role of the estrogen receptor in their development is well established, further research is required to develop a detailed understanding of how its specific isoforms act in different types of cancer.