Evidence map›Paper›PMID 27181033›Full record

ArticleScientific reports2016

α-Amanitin Restrains Cancer Relapse from Drug-Tolerant Cell Subpopulations via TAF15.

Kohei Kume, Miyuki Ikeda, Sawako Miura, Kohei Ito, Kei A Sato, Yukimi Ohmori, Fumitaka Endo, Hirokatsu Katagiri, Kaoru Ishida, Chie Ito and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 33 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

12 authors at 1 institution in 1 country.

Kohei KumeMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Miyuki IkedaMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Sawako MiuraMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Kohei ItoMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Kei A SatoMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Yukimi OhmoriMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Fumitaka EndoMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Hirokatsu KatagiriMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Kaoru IshidaMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Chie ItoMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Takeshi IwayaMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Satoshi S NishizukaMolecular Therapeutics Laboratory, Department of Surgery, Iwate Medical University School of Medicine, Morioka, Iwate 020-8505, Japan.
Iwate Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer relapse occurs with substantial frequency even after treatment with curative intent. Here we studied drug-tolerant colonies (DTCs), which are subpopulations of cancer cells that survive in the presence of drugs. Proteomic characterization of DTCs identified stemness- and epithelial-dominant subpopulations, but functional screening suggested that DTC formation was regulated at the transcriptional level independent from protein expression patterns. We consistently found that α-amanitin, an RNA polymerase II (RNAPII) inhibitor, effectively inhibited DTCs by suppressing TAF15 expression, which binds to RNA to modulate transcription and RNA processing. Sequential administration of α-amanitin and cisplatin extended overall survival in a cancer-relapse mouse model, namely peritonitis carcinomatosa. Therefore, post-treatment cancer relapse may occur through non-distinct subpopulations and may be effectively prevented by α-amanitin to disrupt transcriptional machinery, including TAF15.

Indexed as

Alpha-AmanitinAnimalsCell Line, TumorCisplatinDown-RegulationDrug ResistanceEnzyme InhibitorsGene Expression Regulation, NeoplasticHCT116 CellsHeLa CellsHT29 CellsHumansMCF-7 CellsMicePeritoneal NeoplasmsProteomicsAlpha-AmanitinCisplatinEnzyme InhibitorsTAF15 protein, humanTATA-Binding Protein Associated Factors

Identifiers

PMID27181033
PMCPMC4867652
OpenAlexW2394718431

What OpenQuestion holds

Textmetadata
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.