ArticleCancer medicine2016
LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a.
Article in Cancer medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
- Prognostic values of long noncoding RNA PVT1 in various carcinomas: An updated systematic review and meta-analysis.Cell proliferation · 2018Pooled it
- ncFN: a comprehensive non-coding RNA function annotation framework based on a global and heterogeneous biomolecular network.Non-coding RNA research · 2026Article
- Exploring the oncogenic mechanism of plasmacytoma variant translocation 1 (PVT1) gene in solid cancers; emphasis on microRNA regulation pathways.Cancer cell international · 2026Review
- Combining Serum PVT1 Exon 4A and Exon 9 with Serum Prostate-Specific Antigen Shows Potential for Improving Identification and Risk Stratification of Prostate Cancer.Cancer management and research · 2026Article
- Mechanisms and progress of LncRNAs in prostate cancer development and diagnostic therapy.International urology and nephrology · 2025Review
- LncRNA ZFAS1 promotes the transformation from prostatitis to prostate cancer via myddosome assembly-mediated activation of NF-κB signaling.Discover oncology · 2025Article
- Natural products and long non-coding RNAs in prostate cancer: insights into etiology and treatment resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Neighborhood-Regularized Matrix Factorization for lncRNA-Disease Association Identification.International journal of molecular sciences · 2025Article
- MicroRNAs in bone metastases: mechanisms and research progression.Frontiers in oncology · 2025Review
- The relationship of peripheral blood lncRNA-PVT1 and miR-146a levels with Th17/Treg cytokines in patients with Hashimoto's thyroiditis and their clinical significance.Biomolecules & biomedicine · 2024Article
- MiRNA-146a-A Key Player in Immunity and Diseases.International journal of molecular sciences · 2023Review
- Regulation mechanism and pathogenic role of lncRNA plasmacytoma variant translocation 1 (Genes & diseases · 2023Review
- NInternational journal of oncology · 2023Article
- lncRNA PVT1: a novel oncogene in multiple cancers.Cellular & molecular biology letters · 2022Review
- TheAnnals of translational medicine · 2022Article
- Molecular Landscape of LncRNAs in Prostate Cancer: A focus on pathways and therapeutic targets for intervention.Journal of experimental & clinical cancer research : CR · 2022Review
- Review
- Long non-coding RNA plasmacytoma variant translocation 1 and growth arrest specific 5 regulate each other in osteoarthritis to regulate the apoptosis of chondrocytes.Bioengineered · 2022Article
- Up-regulated lncRNA-PVT1 expression in peripheral blood mononuclear cells of patients with coronary artery disease is correlated with decreased interleukin-10 production.Molecular biology reports · 2022Article
- Long non-coding PRNCR1 regulates the proliferation and apoptosis of synoviocytes in osteoarthritis by sponging miR-377-3p.Journal of orthopaedic surgery and research · 2022Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is the third most common causes of death from cancer in men. Our previous study demonstrated that lncRNA PVT1 was overexpressed and played an oncogenic role in the progression of prostate cancer. However, the molecular mechanism of modulating the prostate cancer tumorigenesis was still unknown. In this study, we aim to investigate the interaction between PVT1 and miR-146a in prostate cancer and reveal the potential mechanism in prostate cancer carcinogenesis. The expression level of miR-146a was assessed by quantitative RT-PCR. The correlation analysis and methylation status analysis was made to confirm the interaction between PVT1 and miR-146a. Biological function analysis was performed through gain-of-function and loss-of-function strategies. Our results showed that miR-146a was downregulated and negatively correlated with PVT1 level in prostate cancer. PVT1 mediated miR-146a expression by inducing the methylation of CpG Island in its promoter. miR-146a overexpression eliminated the effects of PVT1 knockdown on prostate cancer cells. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a. Our study suggested a regulatory relationship between lncRNA PVT1 and miR-146a during the process of the prostate cancer tumorigenesis. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a. It would contribute to the diagnosis, treatment and prognosis of prostate cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.