ArticleThe British journal of dermatology2024
Long noncoding RNA plasmacytoma variant translocation 1 is overexpressed in cutaneous squamous cell carcinoma and exon 2 is critical for its oncogenicity.
Article in The British journal of dermatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Histological and Genetic Markers of Cellular Senescence in Keratinocyte Cancers and Actinic Keratosis: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Spheroids and organoids to study long noncoding RNAs in cancer: how they could replace animal models.Cancer metastasis reviews · 2026Review
- Exploring the oncogenic mechanism of plasmacytoma variant translocation 1 (PVT1) gene in solid cancers; emphasis on microRNA regulation pathways.Cancer cell international · 2026Review
- LncRNA PVT1 in human cancers: genomic complexity, isoforms, functional elements, mechanism of action, subcellular localization and possible role as a therapeutic target.Molecular cancer · 2026Review
- The mechanism of lncRNA PVT1 in oral squamous cell carcinoma.Frontiers in oncology · 2026Review
- LncRNA PVT1 promotes proliferation, migration and invasion of cholangiocarcinoma by regulating the expression of SOCS2.Scientific reports · 2025Article
- A symphony of signals: the intricate role of lncRNAs in dermatological disorders.Clinical and experimental medicine · 2025Review
- Alternative transcription increases isoform complexity in Long Non-Coding RNAs and alters their functions in cancer.Non-coding RNA research · 2025Review
- Endogenous Ribonucleases: Therapeutic Targeting of the Transcriptome Through Oligonucleotide-Triggered RNA Inactivation.Biomolecules · 2025Review
- Molecular Mechanisms and Therapeutic Implications of Long Non-coding RNAs in Cutaneous Biology and Disease.Journal of cellular physiology · 2025Review
- Clustering of RNA co-expression network identifies novel long non-coding RNA biomarkers in squamous cell carcinoma.Scientific reports · 2024Article
- Exon-specific oncogenic function of the long noncoding RNA plasmacytoma variant translocation 1 in cutaneous squamous cell carcinoma: a promising potential therapeutic target.The British journal of dermatology · 2024Article
Corrections and comments
- Commented on by
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- Erratum issuedCorrection.2024
Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundCutaneous squamous cell carcinoma (cSCC) is one of the most common and fastest increasing forms of cancer worldwide with metastatic potential. Long noncoding RNAs (lncRNAs) are a group of RNA molecules with essential regulatory functions in both physiological and pathological processes.
objectivesTo investigate the function and mode of action of lncRNA plasmacytoma variant translocation 1 (PVT1) in cSCC.
methodsQuantitative reverse transcriptase polymerase chain reaction and single-molecule in situ hybridization were used to quantify the expression level of PVT1 in normal skin, premalignant skin lesions, actinic keratosis (AK) and primary and metastatic cSCCs. The function of PVT1 in cSCC was investigated both in vivo (tumour xenografts) and in vitro (competitive cell growth assay, 5-ethynyl-2'-deoxyuridine incorporation assay, colony formation assay and tumour spheroid formation assay) upon CRISPR-Cas9-mediated knockout of the entire PVT1 locus, the knockout of exon 2 of PVT1, and locked nucleic acid (LNA) gapmer-mediated PVT1 knockdown. RNA sequencing analysis was conducted to identify genes and processes regulated by PVT1.
resultsWe identified PVT1 as a lncRNA upregulated in cSCC in situ and cSCC, associated with the malignant phenotype of cSCC. We showed that the expression of PVT1 in cSCC was regulated by MYC. Both CRISPR-Cas9 deletion of the entire PVT1 locus and LNA gapmer-mediated knockdown of PVT1 transcript impaired the malignant behaviour of cSCC cells, suggesting that PVT1 is an oncogenic transcript in cSCC. Furthermore, knockout of PVT1 exon 2 inhibited cSCC tumour growth both in vivo and in vitro, demonstrating that exon 2 is a critical element for the oncogenic role of PVT1. Mechanistically, we showed that PVT1 was localized in the cell nucleus and its deletion resulted in cellular senescence, increased cyclin-dependent kinase inhibitor 1 (p21/CDKN1A) expression and cell cycle arrest.
conclusionsOur study revealed a previously unrecognized role for exon 2 of PVT1 in its oncogenic role and that PVT1 suppresses cellular senescence in cSCC. PVT1 may be a potential biomarker and therapeutic target in cSCC.
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