Evidence map›Paper›PMID 40765796›Full record

ArticleNagoya journal of medical science2025

Long non-coding RNA taurine upregulated 1 regulates the progression of head and neck cancer.

Kohei Nioka, Norihisa Ichimura, Shohei Ikutomi, Hideharu Hibi

Abstract read
In one paragraph

Article in Nagoya journal of medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Kohei NiokaDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Norihisa IchimuraDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shohei IkutomiDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hideharu HibiDepartment of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Taurine upregulated 1 (TUG1), whose function is associated with tumor development, is a relatively new long non-coding RNA. TUG1 is overexpressed in multiple types of cancers. However, in head and neck squamous cell carcinoma (HNSCC), the behavior of TUG1 has not yet been completely elucidated. Therefore, we aimed to clarify the function of TUG1 in HNSCC and develop a novel therapeutic target. We analyzed the expression levels of TUG1 in patients with HNSCC using The Cancer Genome Atlas dataset and human oral keratinocytes, and five HNSCC cell lines (HSC-4, Sa3, HSQ-89, SAS, and Ca9-22) through quantitative reverse-transcription polymerase chain reaction. The biological role of TUG1 in HNSCC was investigated using cell growth and migration assays with antisense oligonucleotides in Ca9-22 and SAS cell lines. TUG1 target genes were identified via microarray analysis. The TUG1 expression level was considerably higher in tumor than in normal tissues, and the same result was observed in human oral keratinocytes and all HNSCC cell lines. TUG1 knockdown dramatically inhibited cell proliferation and migration. Furthermore, we identified nemo-like kinase, which may change in tandem with TUG1 expression. Our findings indicate the possibility for targeting the TUG1-nemo-like kinase axis as a novel approach for the treatment of HNSCC.

Indexed as

Head and Neck NeoplasmsRNA, Long NoncodingSquamous Cell Carcinoma of Head and NeckCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansKeratinocytesRNA, Long NoncodingTUG1 long noncoding RNA, humanhead and neck cancerlong non-coding RNAtaurine upregulated gene1

Identifiers

PMID40765796
PMCPMC12320279

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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.