Evidence map›Paper›PMID 26124179›Full record

ArticleOncotarget2015

Targeting chemotherapy-induced PTX3 in tumor stroma to prevent the progression of drug-resistant cancers.

Jhih-Ying Chi, Yu-Wei Hsiao, Chien-Feng Li, Yu-Chih Lo, Zu-Yau Lin, Jhen-Yi Hong, Yang-Ming Liu, Xiu Han, Shao-Ming Wang, Ben-Kuen Chen and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-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

37 citing papers in PubMed, 73 citations in OpenAlex.

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  11. STAT3 Activates the Pentraxin 3 Gene in Chronic Lymphocytic Leukemia Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022
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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 4 institutions in 1 country.

Jhih-Ying ChiInstitute of Basic Medical Science, National Cheng Kung University, Tainan, Taiwan R.O.C.
Yu-Wei HsiaoInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
Chien-Feng LiDepartment of Pathology, Chi-Mei Medical Center, Tainan, Taiwan R.O.C.
Yu-Chih LoInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
Zu-Yau LinCancer Center and Division of Hepatobiliary Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan R.O.C.
Jhen-Yi HongInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
Yang-Ming LiuInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
Xiu HanInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
Shao-Ming WangInstitute of Basic Medical Science, National Cheng Kung University, Tainan, Taiwan R.O.C.
Ben-Kuen ChenInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
Kelvin K TsaiNational Institute of Cancer Research and Translational Center for Glandular Malignancies, National Health Research Institutes, Tainan, Taiwan R.O.C.
Ju-Ming WangInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan R.O.C.
National Cheng Kung University · TWChi Mei Medical Center · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Health Research Institutes · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor microenvironment has been suggested to participate in tumorigenesis, but the nature of the communication between cancer cells and the microenvironment, especially in response to anticancer drugs, remains obscure. We determined that activation of the CCAAT/enhancer binding protein delta (CEBPD) response to Cisplatin and 5-Fluorouracil in cancer-associated macrophages and fibroblasts contributed to the metastasis, invasion, acquired chemoresistance and stemness of cancer cells by in vitro and in vivo assays. Specifically, reporter and in vivo DNA binding assays were used to determine that Pentraxin 3 (PTX3) is a CEBPD responsive gene and serves a protumor role upon anticancer drug treatment. Finally, a PTX3 peptide inhibitor RI37 was developed and assessed the antitumor effects by in vivo assays. RI37 could function as a promising inhibitor for preventing cancer progression and the metastasis, invasion and progression of drug-resistant cancers. The identification of PTX3 provided a new insight in the interaction between host and tumor and the RI37 peptide showed a great opportunity to largely reduce the risk of invasion and metastasis of cancer and drug-resistant cancers.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsApoptosisCCAAT-Enhancer-Binding Protein-deltaCell Line, TumorCell MovementCell SurvivalCell Transformation, NeoplasticCisplatinC-Reactive ProteinCulture Media, ConditionedDisease ProgressionFemaleFibroblastsFluorouracilAntineoplastic AgentsCCAAT-Enhancer-Binding Protein-deltaCisplatinC-Reactive ProteinCulture Media, ConditionedFluorouracilpentraxin 3 (200-236)PentraxinsPeptide FragmentsSerum Amyloid P-ComponentCAFsCEBPDPTX3TAMstumor microenvironment

Identifiers

PMID26124179
PMCPMC4695165
OpenAlexW1922123666

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.