Evidence map›Paper›PMID 34075561›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2021

Complement factor B regulates cellular senescence and is associated with poor prognosis in pancreatic cancer.

Reiri Shimazaki, Shigetsugu Takano, Mamoru Satoh, Mamoru Takada, Yoji Miyahara, Kosuke Sasaki, Hideyuki Yoshitomi, Shingo Kagawa, Katsunori Furukawa, Tsukasa Takayashiki and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 67 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

16 authors at 3 institutions in 1 country.

Reiri ShimazakiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Shigetsugu TakanoDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan. stakano@faculty.chiba-u.jp.ORCID http://orcid.org/0000-0002-6495-0422
Mamoru SatohDivision of Clinical Mass Spectrometry, Chiba University Hospital, Chiba, 260-8677, Japan.
Mamoru TakadaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Yoji MiyaharaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Kosuke SasakiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Hideyuki YoshitomiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Shingo KagawaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Katsunori FurukawaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Tsukasa TakayashikiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Satoshi KubokiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Kazuyuki SogawaDepartment of Biochemistry, School of Life and Environmental Science, Azabu University, 252-5201, Kanagawa, Japan.
Shinichiro MotohashiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, 260-8677, Chiba, Japan.
Fumio NomuraDivision of Clinical Mass Spectrometry, Chiba University Hospital, Chiba, 260-8677, Japan.
Masaru MiyazakiDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Masayuki OhtsukaDepartment of General Surgery, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba-shi, Chiba, 260- 8677, Japan.
Chiba University · JPChiba University Hospital · JPAzabu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe interplay between cancer cells and stromal components, including soluble mediators released from cancer cells, contributes to the progression of pancreatic ductal adenocarcinoma (PDAC). Here, we set out to identify key secreted proteins involved in PDAC progression.

methodsWe performed secretome analyses of culture media of mouse pancreatic intraepithelial neoplasia (PanIN) and PDAC cells using Stable Isotope Labeling by Amino acid in Cell culture (SILAC) with click chemistry and liquid chromatography-mass spectrometry (LC-MS/MS). The results obtained were verified in primary PDAC tissue samples and cell line models.

resultsComplement factor B (CFB) was identified as one of the robustly upregulated proteins, and found to exhibit elevated expression in PDAC cells compared to PanIN cells. Endogenous CFB knockdown by a specific siRNA dramatically decreased the proliferation of PDAC cells, PANC-1 and MIA PaCa-II. CFB knockdown induced increases in the number of senescence-associated-β-galactosidase (SA-β-gal) positive cells exhibiting p21 expression upregulation, which promotes cellular senescence with cyclinD1 accumulation. Furthermore, CFB knockdown facilitated downregulation of proliferating cell nuclear antigen and led to cell cycle arrest in the G1 phase in PDAC cells. Using immunohistochemistry, we found that high stromal CFB expression was associated with unfavorable clinical outcomes with hematogenous dissemination after surgery in human PDAC patients. Despite the presence of enriched CD8

conclusionsOur data indicate that CFB, a key secreted protein, promotes proliferation by preventing cellular senescence and is associated with immunological tumor promotion in PDAC. These findings suggest that CFB may be a potential target for the treatment of PDAC.

Indexed as

RNA InterferenceAnimalsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationCells, CulturedCellular SenescenceComplement Factor BCyclin-Dependent Kinase Inhibitor p21HumansKaplan-Meier EstimateMiceMultivariate AnalysisPancreatic NeoplasmsPrognosisCDKN1A protein, humanComplement Factor BCyclin-Dependent Kinase Inhibitor p21Complement factor Bp21Pancreatic ductal adenocarcinomaProliferationRegulatory T-cellsSecreted proteinSenescence

Identifiers

PMID34075561
PMCPMC8338870
OpenAlexW3165165362

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.