Abstract
Background: The cause of cervical cancer can be traced to Human Papilloma Virus (HPV) along with other, nonviral factors. The uterine cervix is reactive to hormones, and female hormones have been implicated in cervical cancer pathogenesis. Previous studies have indicated that malignant cervical cells tend to lose Estrogen Receptor alpha (ER-α) expression in the cervical epithelium while maintaining ER-α expression in the stromal cells.
Method: We searched the Web of Science, Embase, PubMed, and Wiley Online Library databases to identify potentially relevant articles up to July 4, 2018. Keywords include uterine cervical neoplasms; receptors, estrogen; estrogen receptor alpha; estrogen receptor modulators; estrogens; cervical cancer and estrogen receptor.
Result: Discussions on molecular transitions and drug therapies offer insights into cervical cancer and the functions of estrogen receptors. We focus on molecular transitions and drug therapies for cervical cancer and ER-α targets. Finally, the targeting of downstream gene products and/or receptors to aid in cervical cancer prevention and therapy is discussed.
Conclusion: Downregulating ER-α expression may be a potential treatment regimen for cervical cancer patients and will be of great significance for patients with cervical cancer who are receiving conventional treatment for nonsurgical treatments.
Keywords: Cervical cancer, estrogen receptor alpha, drug therapy, molecular transitions, Malignant cervical cells, stromal cells.
Graphical Abstract