Evidence map›Paper›PMID 32835591›Full record

ArticleCell cycle (Georgetown, Tex.)2020

Long non-coding RNA UCA1 upregulates KIF20A expression to promote cell proliferation and invasion via sponging miR-204 in cervical cancer.

Qing He, Jianzhou Meng, Shuai Liu, Qiangcheng Zeng, Qinghua Zhu, Zhenlin Wei, Yibo Shao

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 25 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

7 authors at 2 institutions in 1 country.

Qing HeShandong Key Laboratory in University of Functional Bioresource Utilization, College of Life Science, Dezhou University , Dezhou City, Shandong Province, PR. China.
Jianzhou MengInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing City, PR. China.
Shuai LiuShandong Key Laboratory in University of Functional Bioresource Utilization, College of Life Science, Dezhou University , Dezhou City, Shandong Province, PR. China.
Qiangcheng ZengShandong Key Laboratory in University of Functional Bioresource Utilization, College of Life Science, Dezhou University , Dezhou City, Shandong Province, PR. China.
Qinghua ZhuShandong Key Laboratory in University of Functional Bioresource Utilization, College of Life Science, Dezhou University , Dezhou City, Shandong Province, PR. China.
Zhenlin WeiShandong Key Laboratory in University of Functional Bioresource Utilization, College of Life Science, Dezhou University , Dezhou City, Shandong Province, PR. China.
Yibo ShaoShandong Key Laboratory in University of Functional Bioresource Utilization, College of Life Science, Dezhou University , Dezhou City, Shandong Province, PR. China.
Dezhou University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is a female cancer with the second highest motility over the world. It is urgent to find new therapeutic methods based on long-coding RNAs and microRNAs. UCA1 was proved to be related with many human cancer types, but limited researches have been performed for the inner associations between UCA1 and cervical cancer. Eighty females who were undergoing surgeries were recruited for study in our research. We took the cervical cancer tissues and cells from them. Massive experiments and analysis were conducted to investigate the gene expressions and protein expressions about UCA1, KIF20A, and miR-204 in normal cells and cancer cells. The techniques contain real-time PCR, migration/invasion assay, western blot, in vivo experiments, and so on.We found that UCA1 expression was greatly up-regulated in cervical cancer tissues and cell lines. Our in vitro assays revealed that the suppressing of UCA1 could reduce cervical cancer cells proliferation, migration, and invasion. In addition, we found that lncRNA UCA1 could sponge miR-204 and promote the proliferation and invasion of cervical cancer cells via the up-regulating of KIF20A expression. As a result, the inhibiting of UCA1 could lower cervical cancer (CC) cells growth rate in vivo.Our results identified that UCA1 could serve as an oncogene in cervical cancer cell progression through the modulating of miR-204/KIF20A axis. It gives novel insights to the searching of novel therapeutic methods for cervical cancer.

Indexed as

Cell MovementCell ProliferationAdultAnimalsFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansKinesinsMice, NudeMicroRNAsMiddle AgedNeoplasm InvasivenessRNA, Long NoncodingSignal TransductionUterine Cervical NeoplasmsKIF20A protein, humanKinesinsMicroRNAsMIRN204 microRNA, humanRNA, Long NoncodingUCA1 RNA, humancervical cancerKIF20ALncRNA UCA1miR-204

Identifiers

PMID32835591
PMCPMC7553528
OpenAlexW3080912517

What OpenQuestion holds

Textmetadata
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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.