Evidence map›Paper›PMID 26337460›Full record

ArticleJournal of translational medicine2015

MicroRNA-195-5p, a new regulator of Fra-1, suppresses the migration and invasion of prostate cancer cells.

Jian Wu, Alin Ji, Xiao Wang, Yi Zhu, Yasai Yu, Yiwei Lin, Yunfu Liu, Shiqi Li, Zhen Liang, Xin Xu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Review
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  7. Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024
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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

12 authors at 1 institution in 1 country.

Jian WuDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. wujian001x080@163.com.
Alin JiDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. alinjizju@126.com.
Xiao WangDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. 601322528@qq.com.
Yi ZhuDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. emzdnqq@126.com.
Yasai YuDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. yasaisingapore@163.com.
Yiwei LinDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. 21018051@zju.edu.cn.
Yunfu LiuDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. liuyunfuzheyi@126.com.
Shiqi LiDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. josephwoo007@sina.com.
Zhen LiangDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. 583937979@qq.com.
Xin XuDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. zheyishuai@sina.com.
Xiangyi ZhengDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. hexishuiyu@163.com.
Liping XieDepartment of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou, 310003, Zhejiang, China. xielp@zjuem.zju.edu.cn.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAn increasing number of studies have demonstrated that deregulation of microRNAs (miRNAs) was a common event in tumor tissues and miRNAs would be treated as ideal tumor biomarkers or therapeutic targets. miR-195-5p (termed as miR-195 for briefly in the following part) was suggested to function as a tumor suppressor in cancer development and progression. However, the roles of miR-195 in human prostate cancer are still elusive. Thus, this study was performed to investigate the biological functions and its molecular mechanisms of miR-195 in human prostate cancer cell lines, discussing whether it has a potential to be a therapeutic way of prostate cancer.

methodsTwo human prostate cancer cell lines were analyzed for the expression of miR-195 by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR). A gain-of-function study of miR-195 was conducted by transfecting mimics into DU145 and PC3 cells and cell motility and invasion ability were evaluated by wound healing assay and transwell assay. Tissue microarray, and immunohistochemistry with antibodies against Fra-1 was performed using the peroxidase and DAB methods. The target gene of miR-195 was determined by luciferase assay, quantitative RT-PCR and western blot. The regulation of motility by miR-195 was analyzed by western blot.

resultsmiR-195 was frequently down-regulated in both prostate cancer cell lines, DU145 and PC3. Overexpression of miR-195 significantly repressed the capability of migration and invasion of prostate cancer cells. In addition, we identified Fra-1, a cell motility regulator, as a novel target of miR-195. Fra-1 was up-regulated in prostate cancer tissues. We also observed that inhibition of miR-195 or restoration of Fra-1 in miR-195-over-expressed prostate cancer cells partially reversed the suppressive effects of miR-195. Furthermore, we demonstrated miR-195 could inhibit prostate cancer cell motility by regulated the expression of c-Met, MMP1, MMP9.

conclusionsmiR-195 can repress the migration and invasion of prostate cancer cells via regulating Fra-1. Our results indicate that miR-195 could be a tumor suppressor and may have a potential to be a diagnostics or therapeutic target in prostate cancer.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFos-Related Antigen 1HumansMaleMicroRNAsNeoplasm InvasivenessProstatic NeoplasmsProto-Oncogene Proteins c-fosReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTransfection3' Untranslated RegionsFos-Related Antigen 1MicroRNAsMIRN195 microRNA, humanProto-Oncogene Proteins c-fosRNA, Small Interfering

Identifiers

PMID26337460
PMCPMC4558968
OpenAlexW1931923002

What OpenQuestion holds

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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.