Evidence map›Paper›PMID 28582447›Full record

ArticlePloS one2017

Action of YM155 on clear cell renal cell carcinoma does not depend on survivin expression levels.

Mei Yi Sim, Hung Huynh, Mei Lin Go, John Shyi Peng Yuen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 13 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

4 authors at 3 institutions in 1 country.

Mei Yi SimDepartment of Urology, Singapore General Hospital, Republic of Singapore.ORCID http://orcid.org/0000-0001-6546-4699
Hung HuynhLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Republic of Singapore.
Mei Lin GoDepartment of Pharmacy, National University of Singapore, Republic of Singapore.
John Shyi Peng YuenDepartment of Urology, Singapore General Hospital, Republic of Singapore.
Singapore General Hospital · SGNational Cancer Centre Singapore · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dioxonapthoimidazolium YM155 is a survivin suppressant which has been investigated as an anticancer agent in clinical trials. Here, we investigated its growth inhibitory properties on a panel of immortalized and patient derived renal cell carcinoma (RCC) cell lines which were either deficient in the tumour suppressor von Hippel-Lindau (VHL) protein or possessed a functional copy. Neither the VHL status nor the survivin expression levels of these cell lines influenced their susceptibility to growth inhibition by YM155. Of the various RCC lines, the papillary subtype was more resistant to YM155, suggesting that the therapeutic efficacy of YM155 may be restricted to clear cell subtypes. YM155 was equally potent in cells (RCC786.0) in which survivin expression had been stably silenced or overexpressed, implicating a limited reliance on survivin in the mode of action of YM155. A follow-up in-vitro high throughput RNA microarray identified possible targets of YM155 apart from survivin. Selected genes (ID1, FOXO1, CYLD) that were differentially expressed in YM155-sensitive RCC cells and relevant to RCC pathology were validated with real-time PCR and western immunoblotting analyses. Thus, there is corroboratory evidence that the growth inhibitory activity of YM155 in RCC cell lines is not exclusively mediated by its suppression of survivin. In view of the growing importance of combination therapy in oncology, we showed that a combination of YM155 and sorafenib at ½ x IC50 concentrations was synergistic on RCC786.0 cells. However, when tested intraperitoneally on a murine xenograft model derived from a nephrectomised patient with clear cell RCC, a combination of suboptimal doses of both drugs failed to arrest tumour progression. The absence of synergy in vivo highlighted the need to further optimize the dosing schedules of YM155 and sorafenib, as well as their routes of administration. It also implied that the expression of other oncogenic proteins which YM155 may target is either low or absent in this clear cell RCC.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, Renal CellCell Line, TumorCell SurvivalDeubiquitinating Enzyme CYLDDose-Response Relationship, DrugDrug CombinationsForkhead Box Protein O1Gene Expression Regulation, NeoplasticHumansImidazolesInhibitor of Apoptosis ProteinsInhibitor of Differentiation Protein 1Kidney NeoplasmsMaleAntineoplastic AgentsBIRC5 protein, humanCYLD protein, humanDeubiquitinating Enzyme CYLDDrug CombinationsForkhead Box Protein O1FOXO1 protein, humanID1 protein, humanImidazolesInhibitor of Apoptosis ProteinsInhibitor of Differentiation Protein 1NaphthoquinonesNiacinamidePhenylurea CompoundssepantroniumSorafenibSurvivinTumor Suppressor ProteinsVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID28582447
PMCPMC5459331
OpenAlexW2621415659

What OpenQuestion holds

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LicenceCC BY
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.