ArticleJournal of oncology2023
LncRNA PTOV1-AS2 Promotes Colon Cancer Progression through the miR-145-5p/FSCN1 Axis.
Article in Journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- MiR-145 encapsulated small extracellular vesicles inhibit colorectal cancer progression by downregulating fascin actin-bundling protein 1 expression.Stem cell research & therapy · 2025Article
- Noncoding RNA (ncRNA)-mediated regulation of TLRs: critical regulator of inflammation in tumor microenvironment.Medical oncology (Northwood, London, England) · 2025Review
- Exploring the interplay of natural products and long non-coding RNAs in colorectal cancer: pathogenesis, diagnosis, and overcoming drug resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Upregulated PCAT-1 predicts poor prognosis and reduced immune cell infiltration in head and neck squamous cell carcinoma through the miR-145-5p / FSCN-1 axis.Molecular biology reports · 2025Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: The long noncoding RNA (lncRNA) gene PTOV1-AS2 is a potentially oncogenic lncRNA gene. However, its role and regulatory mechanism in the occurrence and development of colon cancer are still unclear. In this study, the lncRNA PTOV1-AS2 was used as a starting point to investigate the role of competing endogenous RNA (ceRNA) regulatory mechanisms in colon cancer. Methods: The expression of lncRNA PTOV1-AS2 mRNA in colon cancer tissues and cell lines was measured by quantitative real-time polymerase chain reaction (qRT-PCR) and screened for differential expression in cells. We examined the effects of lncRNA PTOV1-AS2 overexpression or downregulation of its expression on various cellular processes in HCT116 and SW620 cells after the transfection with an overexpression construct or PTOV1-AS2p-specific shRNA, respectively. In particular, we examined the effects on cell proliferation, migration, and invasion using the cell counting kit-8 CCK-8 assay and Transwell migration and invasion assays, respectively. In addition, the binding targets of lncRNA PTOV1-AS2/miR-145-5p and miR-145-5p/FSCN1 were predicted using various bioinformatics tools and validated by a dual luciferase assay. We also examined the effect of the lncRNA PTOV1-AS2/miR-145-5p axis on FSCN1 expression by qRT-PCR analysis. Furthermore, we investigated the effect of the PTOV1-AS2/miR-145-5p/FSCN1 axis on the biological function of colon cancer cells using an Results: We found that PTOV1-AS2 was highly expressed in colon cancer, which was associated with worse survival. High expression of PTOV1-AS2 promoted cell proliferation, migration, and invasion, while low expression of PTOV1-AS2 inhibited these processes in HCT116 and SW620 cells. The microRNA miR-145-5p was found to bind to the 3'-UTR region of both PTOV1-AS2 and FSCN1. In addition, miR-145-5p decreased the protein expression of its target gene FSCN1 and reduced the PTOV1-AS2-induced expression of FSCN1 in colon cancer cell lines. Also, silencing miR-145-5p or enhancing FSCN1 expression could partially restore the inhibition of cell proliferation, migration, invasion, and the tumorigenic capacity caused by silencing the expression of PTOV1-AS2 Conclusion: PTOV1-AS2 promotes colon cancer progression by "sponging" miR-145-5p to upregulate FSCN1.
Identifiers
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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.