Evidence map›Paper›PMID 28931862›Full record

ArticleScientific reports2017

Long non-coding RNA HOTAIR promotes cell migration by upregulating insulin growth factor-binding protein 2 in renal cell carcinoma.

Hiromichi Katayama, Keiichi Tamai, Rie Shibuya, Mao Nakamura, Mai Mochizuki, Kazunori Yamaguchi, Sadafumi Kawamura, Tatsuo Tochigi, Ikuro Sato, Takamasa Okanishi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  20. Cancers · 2019
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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

14 authors at 3 institutions in 1 country.

Hiromichi KatayamaDivision of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan.
Keiichi TamaiDivision of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan. tamaikeiichi@med.tohoku.ac.jp.
Rie ShibuyaDivision of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan.
Mao NakamuraDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Mai MochizukiDivision of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan.
Kazunori YamaguchiDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Sadafumi KawamuraDepartment of Urology, Miyagi Cancer Center, Natori, Japan.ORCID 0000-0003-3622-2185
Tatsuo TochigiDepartment of Urology, Miyagi Cancer Center, Natori, Japan.
Ikuro SatoDepartment of Pathology, Miyagi Cancer Center, Natori, Japan.
Takamasa OkanishiCenter for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Kunie SakuraiCenter for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Wataru FujibuchiCenter for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Yoichi AraiDepartment of Urology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Kennichi SatohDivision of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan.
Miyagi Prefectural Hospital Organization · JPKyoto University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is one of the most lethal urologic cancers. About one-third of RCC patients already have distal metastasis at the time of diagnosis. There is growing evidence that Hox antisense intergenic RNA (HOTAIR) plays essential roles in metastasis in several types of cancers. However, the precise mechanism by which HOTAIR enhances malignancy remains unclear, especially in RCC. Here, we demonstrated that HOTAIR enhances RCC-cell migration by regulating the insulin growth factor-binding protein 2 (IGFBP2) expression. HOTAIR expression in tumors was significantly correlated with nuclear grade, lymph-node metastasis, and lung metastasis. High HOTAIR expression was associated with a poor prognosis in both our dataset and The Cancer Genome Atlas dataset. Migratory capacity was enhanced in RCC cell lines in a HOTAIR-dependent manner. HOTAIR overexpression accelerated tumorigenicity and lung metastasis in immunodeficient mice. Microarray analysis revealed that IGFBP2 expression was upregulated in HOTAIR-overexpressing cells compared with control cells. The enhanced migration activity of HOTAIR-overexpressing cells was attenuated by IGFBP2 knockdown. IGFBP2 and HOTAIR were co-expressed in clinical RCC samples. Our findings suggest that the HOTAIR-IGFBP2 axis plays critical roles in RCC metastasis and may serve as a novel therapeutic target for advanced RCC.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, Renal CellCell Line, TumorCell MovementFemaleGene Expression ProfilingHumansInsulin-Like Growth Factor Binding Protein 2Kaplan-Meier EstimateKidney NeoplasmsLung NeoplasmsLymphatic MetastasisMaleMice, Inbred NODMice, KnockoutHOTAIR long untranslated RNA, humanInsulin-Like Growth Factor Binding Protein 2RNA, Long Noncoding

Identifiers

PMID28931862
PMCPMC5607269
OpenAlexW2754087347

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.