ArticleJournal of translational medicine2022
MiR-1254 suppresses the proliferation and invasion of cervical cancer cells by modulating CD36.
Article in Journal of translational medicine, 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, 13 citations in OpenAlex.
- Adipocytes in cancer a metabolic paradox and the dawn of novel therapeutics.Discover oncology · 2026Review
- Oroxylin A Directly Targets SRC to Inhibit the PI3K/AKT Signaling Axis in Pancreatic Cancer: An Integrated Bioinformatics and Experimental Study.Biomolecules · 2026Article
- Circular RNAs in cervical cancer: from ceRNA networks to epitranscriptomic regulation, immune modulation, and metastatic reprogramming.Frontiers in immunology · 2026Review
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.Frontiers in immunology · 2026Article
- Regulatory Effect of Non-Coding RNAs on Programmed Cell Death in Melanoma: Novel Therapeutic Crosstalk for Targeted Therapy.Current cancer drug targets · 2026Review
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.bioRxiv : the preprint server for biology · 2025Article
- Aspirin impedes non-small cell lung cancer development via fine-tuning the CD36 localization regulated by GPIHBP1.Translational lung cancer research · 2025Article
- Has_circ_ASH1L acts as a sponge for miR-1254 to promote the malignant progression of cervical cancer by targeting CD36.Cancer gene therapy · 2025Article
- Fatty acid metabolism: A new therapeutic target for cervical cancer.Frontiers in oncology · 2023Review
- The mechanisms and diagnostic potential of lncRNAs, miRNAs, and their related signaling pathways in cervical cancer.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to elucidate the roles of miR-1254 in cervical cancer progression and to explore the underlying mechanisms.
methodsThe expression levels of miR-1254 in normal-cancer cervical tissues and cells were measured using quantitive real-time polymerase chain reaction (qRT-PCR). The invasive and proliferative abilities of cervical cancer cell lines transfected with negative control (NC) mimic or miR-1254 mimic were measured using transwell, CCK-8, and colony formation assays. The binding sites between CD36 and miR-1254 were determined using luciferase reporter assays. The correlation of CD36 and miR-1254 with cervical cancer development was re-confirmed by co-transfection of miR-1254 mimic and CD36 overexpression using CCK-8, colony formation, transwell and western blot assays.
resultsMiR-1254 was expressed at significantly lower levels in the cervical cancer cell lines and tissues than in the controls. The functional assays revealed that upregulation of miR-1254 inhibited the invasion and proliferation of cervical cancer cells. The luciferase reporter assays demonstrated that CD36 messenger RNA and miR-1254 bound to one another. CD36 overexpression reversed the inhibitory effects of upregulated miR-1254 in the cervical cancer cells, suggesting that miR-1254 regulates cervical cancer progression by modulating CD36.
conclusionmiR-1254 attenuated the invasion and proliferation of cervical cancer cells by modulating the expression levels of CD36.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.