Evidence map›Paper›PMID 36012531›Full record

ArticleInternational journal of molecular sciences2022

Senescent Human Pancreatic Stellate Cells Secrete CXCR2 Agonist CXCLs to Promote Proliferation and Migration of Human Pancreatic Cancer AsPC-1 and MIAPaCa-2 Cell Lines.

Tetsuya Takikawa, Shin Hamada, Ryotaro Matsumoto, Yu Tanaka, Fumiya Kataoka, Akira Sasaki, Atsushi Masamune

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

16 citing papers in PubMed, 28 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

7 authors at 1 institution in 1 country.

Tetsuya TakikawaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.ORCID 0000-0002-6214-7337
Shin HamadaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Ryotaro MatsumotoDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Yu TanakaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Fumiya KataokaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.ORCID 0000-0003-2574-886X
Akira SasakiDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.ORCID 0000-0002-2229-9475
Atsushi MasamuneDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.ORCID 0000-0001-7184-7282
Tohoku University · JP

Funding

Japan Society for the Promotion of Science 19K17420 to T.T., 20K08300 to S.H., and 22H03051 to A.M.
6 · The paper itself

Abstract

Interactions between pancreatic cancer cells and pancreatic stellate cells (PSCs) play an important role in the progression of pancreatic cancer. Recent studies have shown that cellular senescence and senescence-associated secretory phenotype factors play roles in the progression of cancer. This study aimed to clarify the effects of senescence-induced PSCs on pancreatic cancer cells. Senescence was induced in primary-cultured human PSCs (hPSCs) through treatment with hydrogen peroxide or gemcitabine. Microarray and Gene Ontology analyses showed the alterations in genes and pathways related to cellular senescence and senescence-associated secretory phenotype factors, including the upregulation of C-X-C motif chemokine ligand (CXCL)-1, CXCL2, and CXCL3 through the induction of senescence in hPSCs. Conditioned media of senescent hPSCs increased the proliferation-as found in an assessment with a BrdU incorporation assay-and migration-as found in an assessment with wound-healing and two-chamber assays-of pancreatic cancer AsPC-1 and MIAPaca-2 cell lines. SB225002, a selective CXCR2 antagonist, and SCH-527123, a CXCR1/CXCR2 antagonist, attenuated the effects of conditioned media of senescent hPSCs on the proliferation and migration of pancreatic cancer cells. These results suggest a role of CXCLs as senescence-associated secretory phenotype factors in the interaction between senescent hPSCs and pancreatic cancer cells. Senescent PSCs might be novel therapeutic targets for pancreatic cancer.

Indexed as

Pancreatic NeoplasmsPancreatic Stellate CellsCell Line, TumorCell ProliferationCellular SenescenceCulture Media, ConditionedHumansReceptors, Interleukin-8BCulture Media, ConditionedReceptors, Interleukin-8Bcancer-associated fibroblastcellular senescencechemokinemyofibroblastpancreatic ductal adenocarcinomasenescence-associated secretory phenotypetumor microenvironment

Identifiers

PMID36012531
PMCPMC9409091
OpenAlexW4292164302

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.