Evidence map›Paper›PMID 30069008›Full record

ArticleCell death & disease2018

Screening for long noncoding RNAs associated with oral squamous cell carcinoma reveals the potentially oncogenic actions of DLEU1.

Koyo Nishiyama, Reo Maruyama, Takeshi Niinuma, Masahiro Kai, Hiroshi Kitajima, Mutsumi Toyota, Yui Hatanaka, Tomohiro Igarashi, Jun-Ichi Kobayashi, Kazuhiro Ogi and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 3 institutions in 1 country.

Koyo NishiyamaDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Reo MaruyamaProject for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Takeshi NiinumaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Masahiro KaiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Hiroshi KitajimaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Mutsumi ToyotaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Yui HatanakaDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Tomohiro IgarashiDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Jun-Ichi KobayashiDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Kazuhiro OgiDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Hironari DehariDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Akihiro MiyazakiDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Akira YorozuDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Eiichiro YamamotoDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Masashi IdogawaDepartment of Medical Genome Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.ORCID 0000-0002-8507-1726
Yasushi SasakiDepartment of Medical Genome Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Tamotsu SugaiDepartment of Molecular Diagnostic Pathology, School of Medicine, Iwate Medical University, Morioka, Japan.
Takashi TokinoDepartment of Medical Genome Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan.
Hiroyoshi HiratsukaDepartment of Oral Surgery, Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
Hiromu SuzukiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, S1, W17, Chuo-ku, Sapporo, 060-8556, Japan. hsuzuki@sapmed.ac.jp.ORCID 0000-0001-9635-3238
Sapporo Medical University · JPIwate Medical University · JPJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that long noncoding RNAs (lncRNAs) have pivotal roles in human malignancies, although their significance in oral squamous cell carcinoma (OSCC) is not fully understood. In the present study, we identified lncRNAs functionally associated with OSCC. By analyzing RNA-seq datasets obtained from primary head and neck squamous cell carcinoma (HNSCC), we identified 15 lncRNAs aberrantly expressed in cancer tissues. We then validated their expression in 18 OSCC cell lines using qRT-PCR and identified 6 lncRNAs frequently overexpressed in OSCC. Among those, we found that knocking down DLEU1 (deleted in lymphocytic leukemia 1) strongly suppressed OSCC cell proliferation. DLEU1 knockdown also suppressed migration, invasion, and xenograft formation by OSCC cells, which is suggestive of its oncogenic functionality. Microarray analysis revealed that DLEU1 knockdown significantly affects expression of a number of cancer-related genes in OSCC cells, including HAS3, CD44, and TP63, suggesting that DLEU1 regulates HA-CD44 signaling. Expression of DLEU1 was elevated in 71% of primary OSCC tissues, and high DLEU1 expression was associated with shorter overall survival of HNSCC patients. These data suggest that elevated DLEU1 expression contributes to OSCC development, and that DLEU1 may be a useful therapeutic target in OSCC.

Indexed as

AnimalsCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMiceMice, NudeMouth NeoplasmsRNA InterferenceRNA, Long NoncodingRNA, Small InterferingTumor Suppressor ProteinsDLEU1 lncRNA, humanRNA, Long NoncodingRNA, Small InterferingTumor Suppressor Proteins

Identifiers

PMID30069008
PMCPMC6070574
OpenAlexW2887554293

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.