Evidence map›Paper›PMID 28271214›Full record

ArticleJournal of cancer research and clinical oncology2017

Long non-coding RNA UCA1 regulates the expression of Snail2 by miR-203 to promote hepatocellular carcinoma progression.

Ji-Nan Xiao, Ting-Hua Yan, Rui-Ming Yu, Yi Gao, Wen-Long Zeng, Sui-Wan Lu, Hua-Xing Que, Ze-Ping Liu, Jin-Hua Jiang

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 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

9 authors at 1 institution in 1 country.

Ji-Nan XiaoDepartment of Radiotherapy, Second Hospital of Longyan City, Longyan, 364000, Fujian, China.
Ting-Hua YanDepartment of Oncology and Internal Medicine, Humanity Hospital of Longyan City, Longyan, 364000, Fujian, China.
Rui-Ming YuDepartment of Oncology and Internal Medicine, Humanity Hospital of Longyan City, Longyan, 364000, Fujian, China.
Yi GaoDepartment of Oncology and Internal Medicine, Humanity Hospital of Longyan City, Longyan, 364000, Fujian, China.
Wen-Long ZengDepartment of Radiotherapy, Second Hospital of Longyan City, Longyan, 364000, Fujian, China.
Sui-Wan LuDepartment of Radiotherapy, Second Hospital of Longyan City, Longyan, 364000, Fujian, China.
Hua-Xing QueDepartment of Radiotherapy, Second Hospital of Longyan City, Longyan, 364000, Fujian, China.
Ze-Ping LiuDepartment of Radiotherapy, Second Hospital of Longyan City, Longyan, 364000, Fujian, China.
Jin-Hua JiangDepartment of Oncology and Internal Medicine, Humanity Hospital of Longyan City, Longyan, 364000, Fujian, China. jiangjinhua1010@163.com.
Longyan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLong non-coding RNA (LncRNA) urothelial carcinoma-associated 1 (UCA1) is reported to be dysregulated in hepatocellular carcinoma (HCC) progression. However, the functions of UCA1 in HCC still need further study. The aim is to detect the role of UCA1 involving in HCC cells proliferation and invasion, and epithelial-mesenchymal transition (EMT).

methodsThe quantitative real-time PCR was used to detect the UCA1 and miR-203 expression levels in 60 cases' HCC tissues and adjacent normal tissues. Western blotting analysis was performed to detect the EMT markers E-cadherin, Vimentin and transcription factor Snail1, Snail2 expression. Luciferase reporter assay, RNA immunoprecipitation (RIP) and pull-down assays were used to evaluate whether miR-203 was a target of UCA1.

resultsOur results showed that UCA1 was markedly upregulated in HCC tissues and higher UCA1 expression in HCC was positively associated with tumor size, vascular invasion and American Joint Committee on Cancer (AJCC) stage (P < 0.05). Furthermore, gain-of-function and loss-of-function analysis showed that UCA1 knockdown inhibited HCC cells proliferation and invasion in vitro and xenograft tumour growth in vivo. Moreover, UCA1 overexpression promoted cell epithelial-mesenchymal transition (EMT) in HCC via effectively sponging to miR-203 and thereby activating the expression of transcription factor Snail2.

conclusionsOur results identified that UCA1/miR-203/Snail2 pathway might involve in HCC progression. Inhibition of UCA1 acted as a promising therapeutic target for HCC patients.

Indexed as

AdultAgedAged, 80 and overAnimalsCarcinoma, HepatocellularCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMicroRNAsMIRN203 microRNA, humanRNA, Long NoncodingSNAI1 protein, humanSnail Family Transcription FactorsUCA1 RNA, humanEpithelial–mesenchymal transitionmiR-203Snail2Urothelial carcinoma-associated 1

Identifiers

PMID28271214
PMCPMC11818964
OpenAlexW2594395199

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.