Evidence map›Paper›PMID 27323817›Full record

ArticleOncotarget2016

The long non-coding RNA HOTAIR increases tumour growth and invasion in cervical cancer by targeting the Notch pathway.

Maria Lee, Hee Jung Kim, Sang Wun Kim, Sun-Ae Park, Kyung-Hee Chun, Nam Hoon Cho, Yong Sang Song, Young Tae Kim

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
8.8field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.

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2 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Maria LeeDepartment of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea.
Hee Jung KimInstitute of Women's Life Medical Science, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea.
Sang Wun KimInstitute of Women's Life Medical Science, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea.
Sun-Ae ParkInstitute of Women's Life Medical Science, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea.
Kyung-Hee ChunDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Korea.
Nam Hoon ChoDepartment of Pathology, Yonsei University College of Medicine, Seoul, Korea.
Yong Sang SongDepartment of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea.
Young Tae KimInstitute of Women's Life Medical Science, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea.
Yonsei University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence suggests that the long non-coding RNA (lncRNA), HOTAIR, is involved in cervical cancer pathogenesis. We examined serum HOTAIR expression levels in cervical cancer patients and determined the relationships between HOTAIR expression and several clinicopathological factors, including survival. We also examined the functional consequences of HOTAIR overexpression both in vitro and in vivo. Compared with control patients, HOTAIR expression was significantly greater in the serum of cervical cancer patients (P < 0.001). The results indicated that this increase was significantly associated with tumour size (P = 0.030), lymphovascular space invasion (P = 0.037), and lymph node metastasis (P = 0.043). Univariate analysis revealed that disease-free survival and overall survival times were significantly shorter in cervical cancer patients with high HOTAIR expression (hazard ratio [HR] = 4.27, 4.68 and P = 0.039, 0.031, respectively). Cell proliferation and invasion in vitro increased as a result of lentiviral-mediated HOTAIR overexpression in cervical cancer cell lines. HOTAIR knockdown inhibited these properties and increased apoptosis. In vivo xenograft experiments using the HOTAIR-overexpressing SiHa cell line revealed that HOTAIR was a strong inducer of tumour growth and modulated the expression of epithelial-mesenchymal transition and Notch-Wnt signalling pathway-related genes. This result suggested that HOTAIR overexpression promoted cell proliferation and invasion. In conclusion, increased HOTAIR expression was associated with decreased patient survival times. HOTAIR may be a useful target for treatment of cervical cancer patients.

Indexed as

Gene Expression Regulation, NeoplasticAdultAnimalsCell Line, TumorFemaleHumansKaplan-Meier EstimateMagnetic Resonance ImagingMice, Inbred BALB CMiddle AgedNeoplasm InvasivenessPositron-Emission TomographyReceptors, NotchRNA, Long NoncodingSignal TransductionTransplantation, HeterologousHOTAIR long untranslated RNA, humanReceptors, NotchRNA, Long Noncodingcervical cancerHOTAIRinvasionlong non-coding RNAprognosis

Identifiers

PMID27323817
PMCPMC5190118
OpenAlexW2424516807

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.