Evidence map›Paper›PMID 35168617›Full record

ArticleJournal of translational medicine2022

Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity.

Xing-Cheng Wu, Yu-Zhong Yu, Yu-Zhi Zuo, Xian-Lu Song, Zhi-En Zhou, Yu Xiao, Dao-Sheng Luo, Wei-Gang Yan, Shan-Chao Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 15 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 5 institutions in 1 country.

Xing-Cheng WuDepartment of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, 100720, China.
Yu-Zhong YuDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yu-Zhi ZuoDepartment of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, 100720, China.
Xian-Lu SongDepartment of Radiotherapy, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Zhi-En ZhouDepartment of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, 100720, China.
Yu XiaoDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Dao-Sheng LuoDepartment of Urology, Dongguan Hospital, Southern Medical University, Guangzhou, China.
Wei-Gang YanDepartment of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, 100720, China. yanweigangpum@sina.com.
Shan-Chao ZhaoDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. zhaoshanchao@263.net.
Peking Union Medical College Hospital · CNNanfang Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNGuangzhou Medical University · CNSouthern Medical University · CN

Funding

national natural science foundation of china 81972394natural science foundation of beijing, china 7192159natural science foundation of beijing, china 7212079natural science foundation of guangdong province 2016A030313583science and technology planning project of guangzhou 201704020070
6 · The paper itself

Abstract

backgroundProstate cancer is the second most common cancer in men, and some new target genes are needed to predict the risk of prostate cancer progression and the treatment.

methodsIn this study, the effects of UAP1L1 (UAP1-like-1) on prostate cancer were investigated by detecting the proliferation, migration, invasion and apoptosis of prostate cancer cells in vitro using MTT, wound healing, Transwell and flow cytometry assay, and the tumor growth in vivo. The downstream genes and pathways of UAP1L1 were explored using Ingenuity Pathway Analysis (IPA), and screened by qRT-PCR and western blot. The effects of CDCA8 on prostate cancer cells were also verified in vitro, which was through detecting the change of proliferation, migration, invasion and apoptosis of prostate cancer cells after CDCA8 knockdown.

resultsThe results indicated that UAP1L1 promoted the proliferation, migration and invasion of prostate cancer cells, which was inhibited by downregulating CDCA8. Furthermore, the promotion of CDCA8 knockdown on cell apoptosis was reduced when UAP1L1 was simultaneously overexpressed.

conclusionsIn conclusion, the results in this study revealed that UAP1L1 promoted the progression of prostate cancer through the downstream gene CDCA8.

Indexed as

Prostatic NeoplasmsApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMaleCDCA8Prostate cancerUAP1L1

Identifiers

PMID35168617
PMCPMC8845250
OpenAlexW4212907701

What OpenQuestion holds

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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 OpenQuestion graph.