Evidence map›Paper›PMID 29532862›Full record

ArticleInternational journal of molecular medicine2018

High glucose induces the proliferation of prostatic cells via downregulating MRE11.

Chunwei Ye, Yi Cai, Qian Cai, Shunhui Yuan, Fan Huang, Xiaofang Yang, Shuchen He, Zhuoheng Li, Yanwen Wang, Delin Yang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
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

11 authors at 2 institutions in 1 country.

Chunwei YeDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Yi CaiDepartment of Urology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Qian CaiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Shunhui YuanDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Fan HuangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Xiaofang YangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Shuchen HeDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Zhuoheng LiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Yanwen WangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Delin YangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Zhipeng LiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Kunming Medical University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the candidate genes and pathways associated with benign prostatic hyperplasia (BPH) and diabetes. In vitro experiments were performed using normal prostatic epithelial RWPE‑1 and HPr‑1 cells. The cell lines were treated with a high‑glucose solution and MTS and bromodeoxyuridine assays were used to assess cell viability. Transcriptome sequencing was used to screen the candidate genes. The expression of candidate genes was further verified by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting. A meiotic recombination 11 (MRE11) overexpression vector was designed and transfected into RWPE‑1 cells to verify the function of MRE11. A streptozotocin‑induced diabetic rat model was established and rat MRE11 levels were determined by RT‑qPCR and immunohistochemical staining. High concentrations of glucose resulted in RWPE‑1 and HPr‑1 cells with high viability. Transcriptome sequencing revealed that MRE11 was downregulated when RWPE‑1 cells were exposed to high‑glucose conditions. When MRE11 was overexpressed, cell viability decreased and cell apoptosis was induced under high‑glucose conditions. Prostatic tissues from rats were collected and assessed; MRE11 expression was observed to be decreased, which was consistent with the in vitro cell experiments. BPH may be associated with diabetes, as MRE11 expression in prostatic cells was decreased when exposed to high‑glucose conditions. Therefore, MRE11 may have potential as a biomarker for the early diagnosis of BPH and diabetes.

Indexed as

AnimalsApoptosisBlotting, WesternCell CycleCell Line, TumorCell ProliferationCell SurvivalHumansImmunohistochemistryIn Vitro TechniquesMaleMRE11 Homologue ProteinProstateProstatic HyperplasiaRatsRats, Sprague-DawleyMRE11 Homologue Protein

Identifiers

PMID29532862
PMCPMC5881645
OpenAlexW2791763981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.