Evidence map›Paper›PMID 30286729›Full record

ArticleBMC cancer2018

Uc.416 + A promotes epithelial-to-mesenchymal transition through miR-153 in renal cell carcinoma.

Yohei Sekino, Naoya Sakamoto, Keisuke Goto, Ririno Honma, Yoshinori Shigematsu, Thang Pham Quoc, Kazuhiro Sentani, Naohide Oue, Jun Teishima, Fumi Kawakami and 4 more

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

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  9. Unveiling ncRNA regulatory axes in atherosclerosis progression.Clinical and translational medicine · 2020
    Review
  10. TUBB3 Reverses Resistance to Docetaxel and Cabazitaxel in Prostate Cancer.International journal of molecular sciences · 2019
    Article
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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 2 countries.

Yohei SekinoDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Naoya SakamotoDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Keisuke GotoCancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI, USA.
Ririno HonmaDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Yoshinori ShigematsuDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Thang Pham QuocDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Kazuhiro SentaniDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Naohide OueDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Jun TeishimaDepartment of Urology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Fumi KawakamiDepartments of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jose A KaramDepartments of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Kanishka SircarDepartments of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Akio MatsubaraDepartment of Urology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Wataru YasuiDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan. wyasui@hiroshima-u.ac.jp.ORCID http://orcid.org/0000-0002-8647-8405
Hiroshima University · JPThe University of Texas MD Anderson Cancer Center · USUniversity of Hawaiʻi at Mānoa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe transcribed ultraconserved regions (T-UCRs) are a novel class of non-coding RNAs that are absolutely conserved across species and are involved in carcinogenesis in some cancers. However, the expression and biological role of T-UCRs in renal cell carcinoma (RCC) remain poorly understood. This study aimed to examine the expression and functional role of Uc.416 + A and analyze the association between Uc.416 + A and epithelial-to-mesenchymal transition in RCC.

methodsExpression of Uc.416 + A in 35 RCC tissues, corresponding normal kidney tissues and 13 types of normal tissue samples was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). We performed a cell growth and migration assay in RCC cell line 786-O transfected with negative control and siRNA for Uc.416 + A. We evaluated the relation between Uc.416 + A and miR-153, which has a complimentary site of Uc.416 + A.

resultsqRT-PCR analysis revealed that the expression of Uc.416 + A was higher in RCC tissues than that in corresponding normal kidney tissues. Inhibition of Uc.416 + A reduced cell growth and cell migration activity. There was an inverse correlation between Uc.416 + A and miR-153. Western blot analysis showed Uc.416 + A modulated E-cadherin, vimentin and snail. The expression of Uc.416 + A was positively associated with the expression of SNAI1, VIM and inversely associated with the expression of CDH1.

conclusionsThe expression of Uc.416 + A was upregulated in RCC and especially in RCC tissues with sarcomatoid change. Uc.416 + A promoted epithelial-to-mesenchymal transition through miR-153. These results suggest that Uc.416 + A may be a promising therapeutic target.

Indexed as

Carcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansKidney NeoplasmsMicroRNAsReverse Transcriptase Polymerase Chain ReactionRNA, UntranslatedMicroRNAsRNA, UntranslatedEpithelial-to-mesenchymal transitionmiR-153Renal cell carcinomaSarcomatoid changeUc.416 + A

Identifiers

PMID30286729
PMCPMC6172711
OpenAlexW2895553517

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.