ArticleThoracic cancer2022
miR-92a-3p promotes breast cancer proliferation by regulating the KLF2/BIRC5 axis.
Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Expression of miR-92a and miR-125b and Their Association with Chemoradiotherapy Response in Locally Advanced Cervical Cancer.International journal of molecular sciences · 2026Article
- The microRNAs landscape of luminal B breast cancer cells in a three-dimensional microenvironment.Hereditas · 2025Article
- KLF13 promotes breast cancer progression through the HTRA1 and the Hedgehog signaling pathway.Breast cancer (Tokyo, Japan) · 2025Article
- Article
- MicroRNA-34a negatively regulates Netrin1 and mediates MEK/ERK pathway to regulate chemosensitivity of gastric cancer cells.Discover oncology · 2024Article
- Choice of blood collection methods influences extracellular vesicles counts and miRNA profiling.Journal of extracellular biology · 2024Article
- UM171 suppresses breast cancer progression by inducing KLF2.Breast cancer research and treatment · 2024Article
- miR-92a-3p promotes pulmonary fibrosis progression by regulating KLF2-mediated endothelial-to-mesenchymal transition.Cytotechnology · 2024Article
- KLF2 is a clinical diagnostic and treatment biomarker of breast cancer.Frontiers in cell and developmental biology · 2023Article
- miR-92a-3p promotes breast cancer proliferation by regulating the KLF2/BIRC5 axis.Thoracic cancer · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer remains the most common malignancy in females around the world. Recently, a growing number of studies have focused on gene dysregulation. In our previous study, Krüppel-like factors (KLFs) were found to play essential roles in breast cancer development, among which KLF2 could function as a tumor suppressor. Nevertheless, the underlying molecular mechanism remains unclear.
methodsmiR-92a-3p was identified as the upstream regulator of KLF2 by starBase v.3.0. The regulation of KLF2 by miR-92a-3p was verified by a series of in vitro and in vivo assays. Further exploration revealed that Baculoviral IAP Repeat Containing 5 (BIRC5) was the target of KLF2. ChIP assay, dual-luciferase reporter analysis, quantitative real-time PCR, and western blot were performed for verification.
resultsmiR-92a-3p functioned as a tumor promoter by inhibiting KLF2 by binding to its 3'-untranslated region (3'-UTR). In addition, KLF2 could transcriptionally suppress the expression of BIRC5.
conclusionCollectively, our results uncovered the miR-92a-3p/KLF2/BIRC5 axis in breast cancer and provided a potential mechanism for breast cancer development, which may serve as promising strategies for breast cancer therapy.
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