ArticleExperimental and therapeutic medicine2021
MicroRNA-615-5p regulates the proliferation and apoptosis of breast cancer cells by targeting HSF1.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Circulating miR-6165 and miR-182-3p as Non-Invasive Biomarkers for Early Detection of Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- HSF1 at the crossroads of chemoresistance: from current insights to future horizons in cell death mechanisms.Frontiers in cell and developmental biology · 2024Review
- Heat Shock Factor 1 Inhibition: A Novel Anti-Cancer Strategy with Promise for Precision Oncology.Cancers · 2023Review
- Article
- Targeting HSF1 for cancer treatment: mechanisms and inhibitor development.Theranostics · 2023Review
- circRNA THBS1 silencing inhibits the malignant biological behavior of cervical cancer cells via the regulation of miR-543/HMGB2 axis.Open medicine (Warsaw, Poland) · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
Breast cancer, which commonly occurs in the epithelium of the mammary gland, is a malignant tumor. MicroRNAs are involved in various cancer-associated processes, and microRNA-615-5p has been identified to be decreased in the pathological tissues from patients with breast cancer. In the present study, the possible mechanism of microRNA-615-5p in the progression of breast cancer was investigated in order to identify potential novel targets for clinical treatment. Heat shock factor 1 (HSF1) was identified as a predictive target gene of microRNA-615-5p using TargetScan analysis. The expression levels of microRNA-615-5p and its target gene, HSF1, were measured in breast cancer tissues and normal adjacent tissues. Additionally, the effects of microRNA-615-5p on MCF-7 breast cancer cell growth and apoptosis were examined. Furthermore, the interaction between HSF1 and microRNA-615-5p was investigated by a dual luciferase gene reporter assay. The expression levels of HSF1 were measured following transfection with microRNA-615-5p or pcDNA3.1-HSF1. Finally, the expression levels of proliferation- and apoptosis-associated factors such as B-cell lymphoma 2 (Bcl-2), cyclin D1, proliferating cell nuclear antigen (PCNA) and bcl-2-like protein 4 (Bax) were determined. The results demonstrated that lower microRNA-615-5p expression and higher HSF1 mRNA expression were present in tumor tissues compared with adjacent tissues (P<0.01). HSF1 was verified as a direct target of microRNA-615-5p using the dual luciferase gene reporter assay. In comparison with untransfected control and mimic-transfected negative control (NC) cells, MCF-7 cells transfected with microRNA-615-5p mimics exhibited reduced cell proliferation and increased apoptosis (P<0.01). However, the overexpression of HSF1 using a vector reversed the suppression of HSF1 induced by microRNA-615-5p mimics (P<0.01). The mRNA and protein expression levels of Bax were significantly increased, whereas those of Bcl-2, cyclin D1 and PCNA were decreased in the cells transfected with microRNA-615-5p mimics compared with the control and NC cells (P<0.01). Collectively, the present study indicated that microRNA-615-5p may mediate the progression of breast cancer by targeting HSF1.
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