Evidence map›Paper›PMID 29660846›Full record

ArticleCancer science2018

Phospholipase D2 promotes disease progression of renal cell carcinoma through the induction of angiogenin.

Shuya Kandori, Takahiro Kojima, Taeko Matsuoka, Takayuki Yoshino, Aiko Sugiyama, Eijiro Nakamura, Toru Shimazui, Yuji Funakoshi, Yasunori Kanaho, Hiroyuki Nishiyama

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Metabolic reprogramming in renal cancer: Events of a metabolic disease.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
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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

10 authors at 2 institutions in 1 country.

Shuya KandoriFaculty of Medicine, Department of Urology, University of Tsukuba, Tsukuba, Japan.ORCID http://orcid.org/0000-0003-4621-8470
Takahiro KojimaFaculty of Medicine, Department of Urology, University of Tsukuba, Tsukuba, Japan.
Taeko MatsuokaFaculty of Medicine, Department of Urology, University of Tsukuba, Tsukuba, Japan.
Takayuki YoshinoFaculty of Medicine, Department of Urology, University of Tsukuba, Tsukuba, Japan.
Aiko SugiyamaDSK Project, Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Eijiro NakamuraDSK Project, Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Toru ShimazuiDepartment of Urology, Ibaraki Prefectural Central Hospital, Kasama, Japan.
Yuji FunakoshiDepartment of Physiological Chemistry, Faculty of Medicine and Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
Yasunori KanahoDepartment of Physiological Chemistry, Faculty of Medicine and Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
Hiroyuki NishiyamaFaculty of Medicine, Department of Urology, University of Tsukuba, Tsukuba, Japan.
University of Tsukuba · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A hallmark of clear cell renal cell carcinoma (ccRCC) is the presence of intracellular lipid droplets (LD) and it is assumed that phosphatidic acid (PA) produced by phospholipase D (PLD) plays some role in the LD formation. However, little is known about the significance of PLD in ccRCC. In this study, we examined the expression levels of PLD in ccRCC. The classical mammalian isoforms of PLD are PLD1 and PLD2, and the levels of both mRNA were higher at the primary tumor sites than in normal kidney tissues. Similarly, both PLD were significantly abundant in tumor cells as determined by analysis using immunohistochemical staining. Importantly, a higher level of PLD was significantly associated with a higher tumor stage and grade. Because PLD2 knockdown effectively suppressed the cell proliferation and invasion of ccRCC as compared with PLD1 in vitro, we examined the effect of PLD2 in vivo. Notably, shRNA-mediated knockdown of PLD2 suppressed the growth and invasion of tumors in nude mouse xenograft models. Moreover, the higher expression of PLD2 was significantly associated with poorer prognosis in 67 patients. As for genes relating to the tumor invasion of PLD2, we found that angiogenin (ANG) was positively regulated by PLD2. In fact, the expression levels of ANG were elevated in tumor tissues as compared with normal kidney and the inhibition of ANG activity with a neutralizing antibody significantly suppressed tumor invasion. Overall, we revealed for the first time that PLD2-produced PA promoted cell invasion through the expression of ANG in ccRCC cells.

Indexed as

Gene Expression Regulation, NeoplasticAgedAnimalsCarcinoma, Renal CellCell Line, TumorDisease ProgressionHEK293 CellsHumansKaplan-Meier EstimateKidney NeoplasmsMice, NudeMiddle AgedPhospholipase DRibonuclease, PancreaticRNA InterferenceRNAi TherapeuticsangiogeninPhospholipase Dphospholipase D2Ribonuclease, Pancreaticangiogenincancer progressionphosphatidic acidphospholipase D2renal cell carcinoma

Identifiers

PMID29660846
PMCPMC5989877
OpenAlexW2800875474

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.