Evidence map›Paper›PMID 33342034›Full record

ArticleMolecular oncology2021

Anti-pyroptotic function of TGF-β is suppressed by a synthetic dsRNA analogue in triple negative breast cancer cells.

Yusuke Tamura, Masato Morikawa, Ryo Tanabe, Kohei Miyazono, Daizo Koinuma

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2021. 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
1.2field-weighted citation impact, top 20% 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, 20 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

5 authors at 1 institution in 1 country.

Yusuke TamuraDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan.
Masato MorikawaDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan.ORCID 0000-0002-6191-7176
Ryo TanabeDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan.
Kohei MiyazonoDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan.
Daizo KoinumaDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan.ORCID 0000-0001-5611-2122
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of innovative therapeutic modalities would address an unmet clinical need in the treatment of triple negative breast cancer (TNBC). Activation of retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) such as melanoma differentiation-associated gene 5 (MDA5) and RIG-I in cancer cells is suggested to suppress tumor progression by inducing cell death. Transfection of polyI:C, a conventionally used synthetic double-stranded RNA (dsRNA) analogue that activates RLRs, has been evaluated in clinical trials. However, detailed mechanisms of tumor suppression by RLRs, especially interactions with other signaling pathways, remain elusive. Here, we showed that transfection of polyI:C suppressed transforming growth factor-β (TGF-β) signaling in a MDA5- and RIG-I-dependent manner. We found that suppression of TGF-β signaling by polyI:C promoted cancer cell death, which was attenuated by forced expression of constitutively active Smad3. More detailed analysis suggested that cell death by polyI:C transfection exhibited characteristics of pyroptosis, which is distinct from apoptosis. Therapeutic efficacy of polyI:C transfection was also demonstrated using a mouse model. These results indicated that intratumor administration of polyI:C and related dsRNA analogues may be promising treatments for TNBC through inhibition of the anti-pyroptotic function of TGF-β.

Indexed as

PyroptosisAnimalsDown-RegulationFemaleHumansMiceMice, Inbred BALB CPoly I-CRNA, Double-StrandedSignal TransductionTHP-1 CellsTransforming Growth Factor betaTriple Negative Breast NeoplasmsTumor Cells, CulturedXenograft Model Antitumor AssaysPoly I-CRNA, Double-StrandedTransforming Growth Factor betapolyI:CpyroptosisRLRTGF-βTNBC

Identifiers

PMID33342034
PMCPMC8096786
OpenAlexW3116724422

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.