ArticleTranslational cancer research2020
MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Senomorphic miR-3155b suppresses the senescence-associated secretory phenotype in therapy-induced senescence.Frontiers in cell and developmental biology · 2026Article
- Assessment of miRNA 106a-5p and 375-3p Expression in the Context of the Wnt/β-Catenin Pathway-Comparison of Prostate Adenocarcinoma and Benign Prostatic Hyperplasia Tissues.International journal of molecular sciences · 2025Article
- AAAGUGC Seed-Containing miRNAs: Master Regulators of Cancer Pathways and Therapeutic Resistance.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- miRNAs Dysregulated in Human Papillomavirus-Associated Benign Prostatic Lesions and Prostate Cancer.Cancers · 2024Article
- Erratum to MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8.Translational cancer research · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor-derived interleukin-8 (IL-8) promotes tumorigenesis and progression of prostate cancer (PCa). MicroRNAs (miRNAs) are noncoding regulatory RNAs and their dysregulation is known to be implicated in carcinogenesis. However, the post-transcriptional mechanism of IL-8 via miRNAs is not fully understood. This study was intended to investigate whether miR-106a could affect the progression of PCa via targeting IL-8 or not.
methodsUsing bioinformatics analysis, we postulated that IL-8 might be post-transcriptionally regulated by miR-106a. This was validated by dual reporter gene assays that miR-106a could bind to the predicted site of IL-8 mRNA. To determine the biological effects of miR-106a on PCa cells (PC-3 and DU145), MTT, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), migration and invasion assays were performed.
resultsWe found that miR-106a was barely expressed in PCa cells, whereas IL-8 was aberrantly upregulated. Elevated miR-106a could reduce IL-8 expression by directly binding the 3'-UTR of IL-8. Overexpression of miR-106a in PCa cells triggered cell apoptosis and suppressed cell proliferation, migration, and invasion.
conclusionsThis research showed that miR-106a could function as a tumor-suppressor by decreasing IL-8 levels in PCa.
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Registered trials
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.