Evidence map›Paper›PMID 31180521›Full record

ArticleInternational journal of oncology2019

PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways.

Zi Yu, Qiang Li, Gejun Zhang, Chengcheng Lv, Qingzhuo Dong, Cheng Fu, Chuize Kong, Yu Zeng

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 12 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

8 authors at 3 institutions in 1 country.

Zi YuDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
Qiang LiDepartment of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
Gejun ZhangDepartment of Urology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Chengcheng LvDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
Qingzhuo DongDepartment of Urology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Cheng FuDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
Chuize KongDepartment of Urology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Yu ZengDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.
China Medical University · CNFirst Hospital of China Medical University · CNLiaoning Cancer Hospital & Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is the most common type of kidney cancer. By analysing The Cancer Genome Atlas (TCGA) database, 16 genes were identified to be consistently highly expressed in RCC tissues compared with the matched para‑tumour tissues. Using a high‑throughput cell viability screening method, it was found that downregulation of only two genes significantly inhibited the viability of 786‑O cells. Among the two genes, pleckstrin homology domain containing O1 (PLEKHO1) has never been studied in RCC, to the best of our knowledge, and its expression level was shown to be associated with the prognosis of patients with RCC in TCGA dataset. The upregulation of PLEKHO1 in RCC was first confirmed in 30 paired tumour and para‑tumour tissues. Then, the effect of PLEKHO1 on cell proliferation and apoptosis was assessed in vitro. Additionally, xenograft tumour models were established to investigate the function of PLEKHO1 in vivo. The results showed that PLEKHO1 knockdown significantly inhibited cell viability and facilitated apoptosis in vitro and impaired tumour formation in vivo. Thus, PLEKHO1 is likely to be associated with the viability of RCC cells in vitro and in vivo. Further gene expression microarray and co‑expression analyses showed that PLEKHO1 may be involved in the serine/threonine‑protein kinase hippo and JNK signalling pathways. Together, the results of the present study suggest that PLEKHO1 may contribute to the development of RCC, and therefore, further study is needed to explore its potential as a therapeutic target.

Indexed as

MAP Kinase Signaling SystemAdultAgedAnimalsCarcinoma, Renal CellCell Line, TumorCell SurvivalFemaleGene Knockdown TechniquesHigh-Throughput Nucleotide SequencingHippo Signaling PathwayHumansIntracellular Signaling Peptides and ProteinsKidney NeoplasmsMaleMiceIntracellular Signaling Peptides and ProteinsPLEKHO1 protein, humanProtein Serine-Threonine KinasesRNA, Messenger

Identifiers

PMID31180521
PMCPMC6561616
OpenAlexW2947515587

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.