Progress in the Understanding of Estrogen Receptor Alpha Signaling in Triple-Negative Breast Cancer: Reactivation of Silenced ER-α and Signaling through ER-α36

三阴性乳腺癌 癌症研究 乳腺癌 雌激素受体 表观遗传学 组蛋白脱乙酰基酶 雌激素受体α 小RNA 癌症 生物 组蛋白 医学 内科学 生物化学 基因
作者
Aya Y. Al-Kabariti,Manal A. Abbas
出处
期刊:Molecular Cancer Research [American Association for Cancer Research]
卷期号:21 (11): 1123-1138 被引量:1
标识
DOI:10.1158/1541-7786.mcr-23-0321
摘要

Triple-negative breast cancer (TNBC) is an aggressive tumor that accounts for approximately 15% of total breast cancer cases. It is characterized by poor prognosis and high rate of recurrence compared to other types of breast cancer. TNBC has a limited range of treatment options that include chemotherapy, surgery, and radiation due to the absence of estrogen receptor alpha (ER-α) rendering hormonal therapy ineffective. However, possible targets for improving the clinical outcomes in TNBC exist, such as targeting estrogen signaling through membranous ER-α36 and reactivating silenced ER-α. It has been shown that epigenetic drugs such as DNA methyltransferase and histone deacetylase inhibitors can restore the expression of ER-α. This reactivation of ER-α, presents a potential strategy to re-sensitize TNBC to hormonal therapy. Also, this review provides up-to-date information related to the direct involvement of miRNA in regulating the translation of ER-α mRNA. Specific epi-miRNAs can regulate ER-α expression indirectly by post-transcriptional targeting of mRNAs of enzymes that are involved in DNA methylation and histone deacetylation. Furthermore, ER-α36, an alternative splice variant of ER-α66, is highly expressed in ER-negative breast tumors and activates MAPK/ERK pathway, promoting cell proliferation, escaping apoptosis, and enhancing metastasis. In the future, these recent advances may be helpful for researchers working in the field to obtain novel treatment options for TNBC, utilizing epigenetic drugs and epi-miRNAs that regulate ER-α expression. Also, there is some evidence to suggest that drugs that decrease the expression of ER-α36 may be effective in treating TNBC.
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