Evidence map›Paper›PMID 34785680›Full record

ArticleScientific reports2021

Apoptosis-associated speck-like protein containing a CARD regulates the growth of pancreatic ductal adenocarcinoma.

Mitsuhito Koizumi, Takao Watanabe, Junya Masumoto, Kotaro Sunago, Yoshiki Imamura, Kozue Kanemitsu, Teru Kumagi, Yoichi Hiasa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
2.5field-weighted citation impact, top 9% 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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  7. Journal of medicine and life · 2024
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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 1 institution in 1 country.

Mitsuhito KoizumiDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Takao WatanabeDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Junya MasumotoDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science Center, Ehime, Japan.
Kotaro SunagoDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Yoshiki ImamuraDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Kozue KanemitsuDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Teru KumagiDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Yoichi HiasaDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan. hiasa@m.ehime-u.ac.jp.
Ehime University · JP

Funding

Japan Society for the Promotion of Science JP18K15819
6 · The paper itself

Abstract

Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) is a key adaptor protein of inflammasomes and a proapoptotic molecule; however, its roles in signal transduction in pancreatic ductal adenocarcinoma (PDAC) cells remain unknown. Here, we clarified the role and mechanisms of action of ASC in PDAC using clinical evidence and in vitro data. ASC expression in PDAC tissues was analyzed using public tumor datasets and immunohistochemistry results of patients who underwent surgery, and PDAC prognosis was investigated using the Kaplan-Meier Plotter. ASC expression in PDAC cells was downregulated using small-interfering RNA, and gene expression was assessed by RNA sequencing. Review of the Oncomine database and immunostaining of surgically removed tissues revealed elevated ASC expression in PDAC tumors relative to non-tumor tissue, indicating poor prognosis. We observed high ASC expression in multiple PDAC cells, with ASC silencing subsequently inhibiting PDAC cell growth and altering the expression of cell cycle-related genes. Specifically, ASC silencing reduced cyclin D1 levels and stopped the cell cycle at the G1 phase but did not modulate the expression of any apoptosis-related molecules. These results show that ASC inhibited tumor progression via cell cycle modulation in PDAC cells and could be a potential therapeutic target.

Indexed as

Carcinoma, Pancreatic DuctalCARD Signaling Adaptor ProteinsGene Expression Regulation, NeoplasticNeoplasm ProteinsPancreatic NeoplasmsCell Line, TumorDisease-Free SurvivalFemaleHumansMaleSurvival RateCARD Signaling Adaptor ProteinsNeoplasm ProteinsPYCARD protein, human

Identifiers

PMID34785680
PMCPMC8595714
OpenAlexW3211362032

What OpenQuestion holds

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Registered trials

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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.