Evidence map›Paper›PMID 30864678›Full record

ArticleInternational journal of molecular medicine2019

URG11 promotes proliferation and induced apoptosis of LNCaP cells.

Chenmin Sun, Guangming Zhang, Shujie Cheng, Haining Qian, Dong Li, Min Liu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Journal of men's health · 2022
    Article
  2. Article
  3. 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

6 authors at 2 institutions in 1 country.

Chenmin SunDepartment of Anesthesiology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China.
Guangming ZhangDepartment of Anesthesiology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China.
Shujie ChengDepartment of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China.
Haining QianDepartment of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China.
Dong LiDepartment of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China.
Min LiuDepartment of Urology, Tongren Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200336, P.R. China.
Tongren Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

von Willebrand factor C and EGF domain‑containing protein (URG11), a cell growth regulator, is involved in the progression of a variety of types of cancer, including prostate cancer (Pca). However, the functions of the URG11 gene in Pca cells require in‑depth investigation. The mRNA and protein levels of URG11 were measured by reverse transcription quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. Cell Counting kit‑8 (CCK‑8), wound‑healing and Transwell assays were used to detect cell viability, migration and invasion, respectively. Apoptosis and cell cycle analyses were performed using flow cytometry. The mRNA and protein expression levels of epithelial (E)‑cadherin, vimentin, α‑smooth muscle actin (α‑SMA), cyclin D1 and MYC proto‑oncogene protein (c‑Myc) were analyzed by RT‑qPCR and western blot analysis. In the present study, the mRNA and protein levels of URG11 were markedly upregulated in Pca cell lines compared with those in the normal prostate epithelial cell line. With functional experiments, the cell viability, migration and invasion of Pca cells were markedly promoted by URG11 overexpression. The cell cycle was effectively induced by URG11 and apoptosis was inhibited by the overexpression of URG11. Concomitantly, the epithelial marker E‑cadherin was downregulated, and the mesenchymal markers vimentin and α‑SMA were upregulated following URG11 overexpression. By contrast, genetic knockout of URG11 elicited the opposite effects. The present study also identified that the downstream effector genes of the Wnt/β‑catenin signal pathway, cyclin D1 and c‑Myc, were increased following the overexpression of endogenous URG11, which are known to regulate cell proliferation. In addition, the Wnt/β‑catenin inhibitor FH535 ameliorated the promotive effects of URG11 on LNCaP cells viability, migration and invasion, and the Wnt/β‑catenin agonist LiCl reversed the inhibitory effects of siURG11 in LNCaP cells on cell viability, migration and invasion. The present study demonstrated that URG11 served an oncogenic role in the development of Pca cells and provided evidence that URG11 has potential as a novel therapeutic target in Pca.

Indexed as

ApoptosisActinsCadherinsCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationCell SurvivalCyclin D1Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansLithium ChlorideMaleNeoplasm InvasivenessProstatic NeoplasmsACTA2 protein, humanActinsCadherinsCCND1 protein, humanCyclin D1FH535Lithium ChlorideProto-Oncogene Proteins c-mycRNA, Small InterferingSulfonamidesTrans-ActivatorsVimentinVWCE protein, human

Identifiers

PMID30864678
PMCPMC6443344
OpenAlexW2920198911

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.