ArticleAging2021
METTL3-mediated m6A modification of KIF3C-mRNA promotes prostate cancer progression and is negatively regulated by miR-320d.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 46 citations in OpenAlex.
- RNA methylation in urological cancers: regulatory logic, biological functions, and clinical relevance.Frontiers in immunology · 2026Review
- miR-320d Is Associated with Reduced Nasopharyngeal Carcinoma Progression, Potentially through the NF-κB/IL-8 Axis-Mediated Inhibition of Neutrophil Extracellular Trap Formation.Oncology research · 2026Article
- The emerging role of mFrontiers in immunology · 2026Review
- Emerging implications of N6-methyladenosine in prostate cancer progression and treatment.Cell death discovery · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Components of the Endosome-Lysosome Vesicular Machinery as Drivers of the Metastatic Cascade in Prostate Cancer.Cancers · 2024Review
- Stabilization of RRBP1 mRNA via an mCellular and molecular life sciences : CMLS · 2024Article
- Overview of the interplay between m6A methylation modification and non-coding RNA and their impact on tumor cells.Translational cancer research · 2024Review
- Role of NOncology reports · 2024Review
- Article
- MUC20 regulated by extrachromosomal circular DNA attenuates proteasome inhibitor resistance of multiple myeloma by modulating cuproptosis.Journal of experimental & clinical cancer research : CR · 2024Article
- Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024Review
- The role of the methyltransferase METTL3 in prostate cancer: a potential therapeutic target.BMC cancer · 2024Review
- The functions and mechanisms of RNA modification in prostate: Current status and future perspectives.Frontiers in genetics · 2024Review
- The role of RNA modification in urological cancers: mechanisms and clinical potential.Discover oncology · 2023Review
- Multilevel regulation of NGenes & diseases · 2023Review
- The emerging roles and mechanism of N6-methyladenosine (mFrontiers in pharmacology · 2023Review
- Emerging Mutual Regulatory Roles between mInternational journal of molecular sciences · 2023Review
- Crosstalk between mOncogene · 2022Review
- Functions and mechanisms of N6‑methyladenosine in prostate cancer (Review).Molecular medicine reports · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The occurrence of distant metastasis is one of the leading causes of death in patients with prostate cancer (PCa). It is confirmed that kinesin protein is associated with a variety of malignancies, and the KIF3 family is related to cancer, but the relationship between KIF3C and prostate cancer is not clear. Our experiments have confirmed that KIF3C is highly expressed in prostate cancer tissues and cell lines. Further, functional tests have proven that KIF3C can promote the growth migration and invasion of PCa. We used Starbase 3.0 to discover that methyltransferase like 3 (METTL3) interacts with KIF3C. Our hypothesis and experiments concluded that METTL3 induced m6A modification on KIF3C, promoting the stabilization of KIF3C-mRNA by IGF2 binding protein 1 (IGF2BP1). The prediction that miR-320d inhibits KIF3C expression by targeting METTL3 using the miRmap website, was later confirmed experimentally. Further, a recovery experiment was used to confirm that miR-320d inhibited the progression of prostate cancer. KIF3C was overexpressed in prostate cancer, promoting its growth migration and invasion was induced by miR-320d/METTL3 in an m6A dependent process.
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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.