ArticleCancer gene therapy2023
LncNAP1L6 activates MMP pathway by stabilizing the m6A-modified NAP1L2 to promote malignant progression in prostate cancer.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
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- The role of m6A methylation in abdominal aortic aneurysms: Mechanisms, progress and future perspectives (Review).Molecular medicine reports · 2025Review
- Bone metastases of prostate cancer: Molecular mechanisms, targeted diagnosis and targeted therapy (Review).Oncology reports · 2025Review
- Resolving the current controversy of use and reuse of housekeeping proteins in ageing research: Focus on saving people's tax dollars.Ageing research reviews · 2024Review
- Role of N6-methyladenosine in tumor neovascularization.Cell death & disease · 2024Review
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- mAging and disease · 2024Article
- LOXL1-AS1 inhibits JAK2 ubiquitination and promotes cholangiocarcinoma progression through JAK2/STAT3 signaling.Cancer gene therapy · 2024Article
- The regulatory process and practical significance of non-coding RNA in the dissemination of prostate cancer to the skeletal system.Frontiers in oncology · 2024Review
- Methyltransferase-like proteins in cancer biology and potential therapeutic targeting.Journal of hematology & oncology · 2023Review
- Review
- Long non-coding RNAs in bone metastasis: progresses and perspectives as potential diagnostic and prognostic biomarkers.Frontiers in endocrinology · 2023Review
- The mFrontiers in immunology · 2023Article
- Regulation and Therapeutic Application of Long non-Coding RNA in Tumor Angiogenesis.Technology in cancer research & treatmentReview
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant progression such as bone metastasis, which is associated with pathologic fractures, pain and reduced survival frequently occurs in prostate cancer (PCa) patients at advanced stages. Accumulating evidence has supported that long non-coding RNAs (lncRNAs) participate in multiple biological processes. Nevertheless, the functions of most lncRNAs in PCa malignant progression remain largely unclear. Our current study is to elucidate the influence of lncRNA lncNAP1L6 on PCa malignant progression and uncover the possible regulatory mechanism. Firstly, RT-qPCR analysis was to detect lncNAP1L6 expression and suggested that lncNAP1L6 was markedly upregulated in PCa cells. Functional assays manifested that silencing of lncNAP1L6 hampered cell migration, invasion, and epithelial-mesenchymal transition (EMT) while overexpression of lncNAP1L6 exacerbated cell migration, invasion and EMT. In addition, mechanism assays were to determine the latent regulatory mechanism of lncNAP1L6. It turned out that METTL14/METTL3 complex mediated m6A methylation of NAP1L2 mRNA. Besides, lncNAP1L6 recruited HNRNPC to m6A-modified NAP1L2, leading to stabilization of NAP1L2 mRNA. Moreover, NAP1L6 interacted with YY1 to promote the transcription of MMP2 and MMP9 and activate MMP signaling pathway. In summary, lncNAP1L6 was identified as an oncogene in PCa, which revealed that lncNAP1L6 might be used as potential therapeutic target in PCa.
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