Evidence map›Paper›PMID 25609195›Full record

ArticleBMC cancer2015

Downregulation of EphA5 by promoter methylation in human prostate cancer.

Shibao Li, Yingfeng Zhu, Chunguang Ma, Zhenhua Qiu, Xinju Zhang, Zhihua Kang, Zhiyuan Wu, Hua Wang, Xiao Xu, Hu Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 80 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

14 authors at 4 institutions in 1 country.

Shibao LiDepartment of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, 12 Central Urumqi Road, Shanghai, 200040, China. sdjnshlb@126.com.
Yingfeng ZhuDepartment of Pathology, Huashan Hospital North, Fudan University, Shanghai, China. zhubona@qq.com.
Chunguang MaDepartment of Urology, Fudan University Shanghai Cancer Center, Shanghai, China. machunguang@sohu.com.
Zhenhua QiuDepartment of Laboratory Medicine, The people's hospital of GaoZhou, GaoZhou, China. 345273895@qq.com.
Xinju ZhangCentral Laboratory, Huashan Hospital, Shanghai Medical School, Fudan University, Shanghai, China. pp_dou@163.com.
Zhihua KangDepartment of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, 12 Central Urumqi Road, Shanghai, 200040, China. kangban@163.com.
Zhiyuan WuDepartment of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, 12 Central Urumqi Road, Shanghai, 200040, China. wuzhiyuan126@126.com.
Hua WangDepartment of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, 12 Central Urumqi Road, Shanghai, 200040, China. nausicaa.dx@live.cn.
Xiao XuCentral Laboratory, Huashan Hospital, Shanghai Medical School, Fudan University, Shanghai, China. nausicaadx@163.com.
Hu ZhangDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China. zhh_888666@126.com.
Guoqiang RenDepartment of Pathology, Huashan Hospital North, Fudan University, Shanghai, China. rentta@163.com.
Jianmin TangDepartment of Pathology, Huashan Hospital North, Fudan University, Shanghai, China. tjm195925@163.com.
Xiangyu LiDepartment of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, 12 Central Urumqi Road, Shanghai, 200040, China. lxy_2006000@126.com.
Ming GuanDepartment of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, 12 Central Urumqi Road, Shanghai, 200040, China. guanming88@yahoo.com.
Huashan Hospital · CNFudan University · CNFudan University Shanghai Cancer Center · CNGaozhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEphA5 is a member of the Eph/ephrin family and plays a critical role in the regulation of carcinogenesis. A significant reduction of EphA5 transcripts in high-grade prostate cancer tissue was shown using a transcriptomic analysis, compared to the low-grade prostate cancer tissue. As less is known about the mechanism of EphA5 downregulation and the function of EphA5, here we investigated the expression and an epigenetic change of EphA5 in prostate cancer and determined if these findings were correlated with clinicopathologic characteristics of prostate cancer.

methodsSeven prostate cell lines (RWPE-1, LNCap, LNCap-LN3, CWR22rv-1, PC-3, PC-3M-LN4, and DU145), thirty-nine BPH, twenty-two primary prostate carcinomas, twenty-three paired noncancerous and cancerous prostate tissues were examined via qRT-PCR, methylation-specific PCR, bisulfite sequencing, immunohistochemistry and western blotting. The role of EphA5 in prostate cancer cell migration and invasion was examined by wound healing and transwell assay.

resultsDownregulation or loss of EphA5 mRNA or protein expression was detected in 28 of 45 (62.2%) prostate carcinomas, 2 of 39 (5.1%) hyperplasias, and all 6 prostate cancer cell lines. Methylation of the EphA5 promoter region was present in 32 of 45 (71.1%) carcinoma samples, 3 of 39 (7.7%) hyperplasias, and the 6 prostate cancer cell lines. Among 23 paired prostate carcinoma tissues, 16 tumor samples exhibited the hypermethylation of EphA5, and 15 of these 16 specimens (93.8%) shown the downregulation of EphA5 expression than that of their respectively matched noncancerous samples. Immunostaining analysis demonstrated that the EphA5 protein was absent or down-regulated in 10 of 13 (76.9%) available carcinoma samples, and 8 of these 10 samples (80.0%) exhibited hypermethylation. The frequency of EphA5 methylation was higher in cancer patients with an elevated Gleason score or T3-T4 staging. Following the treatment of 6 prostate cancer cell lines with 5-aza-2'-deoxycytidine, the levels of EphA5 mRNA were significantly increased. Prostate cancer cells invasion and migration were significantly suppressed by ectopic expression of EphA5 in vitro.

conclusionOur study provides evidence that EphA5 is a potential target for epigenetic silencing in primary prostate cancer and is a potentially valuable prognosis predictor and thereapeutic marker for prostate cancer.

Indexed as

AgedBiomarkers, TumorCell Line, TumorDNA MethylationGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm StagingPromoter Regions, GeneticProstatic NeoplasmsReceptor, EphA5RNA, MessengerBiomarkers, TumorEPHA5 protein, humanReceptor, EphA5RNA, Messenger

Identifiers

PMID25609195
PMCPMC4307617
OpenAlexW2093629649

What OpenQuestion holds

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LicenceCC BY
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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.