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miR-378a-3p modulates tamoxifen sensitivity in breast cancer MCF-7 cells through targeting GOLT1A
Kazuhiro Ikeda1, Kuniko Horie-Inoue1, Toshihide Ueno2
1Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Abstract:
Breast cancer is a hormone-dependent cancer and usually treated with endocrine therapy using aromatase inhibitors or anti-estrogens such as tamoxifen. A majority of breast cancer, however, will often fail to respond to endocrine therapy. In the present study, we explored miRNAs associated with endocrine therapy resistance in breast cancer. High-throughput miRNA sequencing was performed using RNAs prepared from breast cancer MCF-7 cells and their derivative clones as endocrine therapy resistant cell models, including tamoxifen-resistant (TamR) and long-term estrogen-deprived (LTED) MCF-7 cells. Notably, miR-21 was the most abundantly expressed miRNA in MCF-7 cells and overexpressed in TamR and LTED cells. We found that miR-378a-3p expression was downregulated in TamR and LTED cells as well as in clinical breast cancer tissues. Additionally, lower expression levels of miR-378a-3p were associated with poor prognosis for tamoxifen-treated patients with breast cancer. GOLT1A was selected as one of the miR-378a-3p candidate target genes by in silico analysis. GOLT1A was overexpressed in breast cancer specimens and GOLT1A-specific siRNAs inhibited the growth of TamR cells. Low GOLT1A levels were correlated with better survival in patients with breast cancer. These results suggest that miR-378a-3p-dependent GOLT1A expression contributes to the mechanisms underlying breast cancer endocrine resistance.
Insights
MicroRNAs like miR-378a-3p are crucial in breast cancer endocrine therapy resistance. Downregulation of miR-378a-3p and its target GOLT1A may drive resistance to tamoxifen, impacting patient prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Breast cancer is often hormone-dependent, treated with endocrine therapy.
- Many breast cancers develop resistance to endocrine therapies like tamoxifen.
- Understanding resistance mechanisms is vital for improving treatment outcomes.
Purpose of the Study:
- To investigate microRNAs (miRNAs) associated with endocrine therapy resistance in breast cancer.
- To identify specific miRNAs and their target genes involved in tamoxifen resistance.
Main Methods:
- High-throughput miRNA sequencing on MCF-7 cells and resistant models (tamoxifen-resistant and long-term estrogen-deprived).
- In silico analysis to predict miRNA targets.
- Validation in clinical breast cancer tissues and cell growth assays.
Main Results:
- miR-21 was highly expressed in all tested breast cancer cells.
- miR-378a-3p was downregulated in resistant cells and tissues, correlating with poor tamoxifen treatment prognosis.
- GOLT1A, a target of miR-378a-3p, was overexpressed and its inhibition slowed resistant cell growth.
- Low GOLT1A levels predicted better patient survival.
Conclusions:
- miR-378a-3p downregulation contributes to endocrine therapy resistance in breast cancer.
- The miR-378a-3p/GOLT1A axis plays a role in tamoxifen resistance mechanisms.
- Targeting the miR-378a-3p/GOLT1A pathway may offer new therapeutic strategies for resistant breast cancer.
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