ArticleInternational journal of molecular sciences2024
Delving into the Role of lncRNAs in Papillary Thyroid Cancer: Upregulation of LINC00887 Promotes Cell Proliferation, Growth and Invasion.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- LncRNA OIP5-AS1 knockdown is associated with attenuated nonylphenol-induced cardiac fibrosis.Environmental health and preventive medicine · 2026Article
- UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma.Frontiers in immunology · 2026Article
- Knockdown of LRP11-AS1 inhibits papillary thyroid tumor growth by modulating miR-615-3p/AKT2 axis.Translational oncology · 2025Article
- The Interplay Between lncRNAs-microRNAs Network Dysregulation and Cellular Hallmarks of Thyroid Cancer.Cancers · 2025Review
- Dual roles of long non-coding RNAs in thyroid cancer: regulation of programmed cell death pathways.Medical oncology (Northwood, London, England) · 2025Review
- Environmental Exposure to Bisphenol A Enhances Invasiveness in Papillary Thyroid Cancer.International journal of molecular sciences · 2025Article
- The regulatory network of epithelial-mesenchymal transition-associated non-coding RNAs in thyroid cancer: molecular mechanisms, clinical implications, and therapeutic strategies.Frontiers in oncology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
Papillary thyroid carcinoma (PTC) is the most common histological category of thyroid cancer. In recent years, there has been an increasing number of studies on lncRNAs in PTC. Long intergenic non-protein coding RNA 887 (LINC00887) is a critical oncogene in developing other cancers. LINC00887 is upregulated in PTC samples but its role in PTC is currently unclear. This study aimed to investigate the impact the disruption of LINC00887 expression has on PTC progression. We performed a CRISPR/Cas9 strategy for the truncation of LINC00887 in BCPAP and TPC1 cell lines. Functional assays showed that LINC00887 knockdown in both TPC1 and BCPAP cells reduced cell proliferation, colony formation and migration, delayed the cell cycle, and increased apoptosis. These results strengthened the role of LINC00887 in cancer and showed for the first time that this lncRNA could be a potential oncogene in PTC, acting as a tumor promoter. Modulation of the immune system may be one of the etiopathogenic mechanisms of LINC00887 in PTC, as shown by the observed influence of this lncRNA on PD-L1 expression. In addition, the biological pathways of LINC00887 identified to date, such as EMT, the Wnt/β-catenin signaling pathway or the FRMD6-Hippo signaling pathway may also be relevant regulatory mechanisms operating in PTC.
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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 Socratic graph.