ArticleMolecular cancer2018
Estrogen-induced miR-196a elevation promotes tumor growth and metastasis via targeting SPRED1 in breast cancer.
Article in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 87 citations in OpenAlex.
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- IFN-γ enhances the therapeutic efficacy of MSCs-derived exosome via miR-126-3p in diabetic wound healing by targeting SPRED1.Journal of diabetes · 2024Article
- Long noncoding RNA LOC646029 functions as a ceRNA to suppress ovarian cancer progression through the miR-627-3p/SPRED1 axis.Frontiers of medicine · 2023Article
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- Obesity as a Risk Factor for Breast Cancer-The Role of miRNA.International journal of molecular sciences · 2022Review
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- Tumor-derived miR-130b-3p induces cancer-associated fibroblast activation by targeting SPIN90 in luminal A breast cancer.Oncogenesis · 2022Article
- Rhein promotes the proliferation of keratinocytes by targeting oestrogen receptors for skin ulcer treatment.BMC complementary medicine and therapies · 2022Article
- Comprehensive functional genomic analyses link APC somatic mutation and mRNA-miRNA networks to the clinical outcome of stage-III colorectal cancer patients.Biomedical journal · 2022Observational
- miR-196a Upregulation Contributes to Gefitinib Resistance through Inhibiting GLTP Expression.International journal of molecular sciences · 2022Article
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- MicroRNA signature in classical Hodgkin lymphoma.Journal of applied genetics · 2021Review
- Hypoxia-inducible miR-196a modulates glioblastoma cell proliferation and migration through complex regulation of NRAS.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- The diagnostic and prognostic values of microRNA-196a in cancer.Bioscience reports · 2021Article
- PUM1 Is Overexpressed in Colon Cancer Cells With Acquired Resistance to Cetuximab.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundEstrogen plays a critical role in breast cancer (BC) progression through estrogen receptor (ER)-mediated gene regulation. Emerging studies suggest that the malignant progress of BC cells is influenced by the cross talk between microRNAs (miRNAs) and ER-α signaling. However, the mechanism and functional linkage between estrogen and miRNAs remain unclear.
methodsThe expression levels of miR-196a and SPRED1 in BC were tested by qRT-PCR in 46 paired BC and adjacent tissues and by the GEO datasets. The role of miR-196a in estrogen-induced BC development was examined by CCK-8 assay, wound healing assay, Matrigel invasion assay and tumorigenicity assay in nude mice. The binding site of ER-α in miR-196a promoter region was analyzed by ChIP-seq, ChIP assay and luciferase reporter assay. The potential targets of miR-196a in BC cells were explored using the luciferase reporter assay and western blot analysis, and the correlation between miR-196a and SPRED1 was analyzed by Spearman's correlation analysis in BC specimens and GEO dataset. TCGA BRCA data was used to characterize the ESR1 signatures according to MSigDB gene set.
resultsThe expression levels of miR-196a were higher in ER-positive (ER+) breast tumors compared to ER-negative (ER-) tumor tissue samples. Besides, miR-196a was involved in estrogen-induced BC cell proliferation, migration and invasion. Notably, the up-regulation of miR-196a was mediated by a direct interaction with estrogen receptor α (ER-α) but not estrogen receptor β (ER-β) in its promoter region, and miR-196a expression levels were positively correlated to ER-α signature scores. Furthermore, SPRED1 was a new direct target of miR-196a which participated in miR-196a-promoted BC development and was suppressed by ligand-activated ER-α signal pathway. Finally, forced expression of miR-196a induced tumor growth of MCF7 cells, while inhibition of miR-196a significantly suppressed the tumor progress in vivo.
conclusionsOverall, the identification of estrogen/miR-196a/SPRED1 cascade will shed light on new molecular mechanism of estrogen signaling in BC development and therapy.
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