Evidence map›Paper›PMID 33893076›Full record

ArticleCancer genomics & proteomics

Desmoplastic Crosstalk in Pancreatic Ductal Adenocarcinoma Is Reflected by Different Responses of Panc-1, MIAPaCa-2, PaTu-8902, and CAPAN-2 Cell Lines to Cancer-associated/Normal Fibroblasts.

Štepán Novák, Michal Kolář, Arpád Szabó, Zdena Vernerová, Lukáš Lacina, Hynek Strnad, Jana Šáchová, Miluše Hradilová, Jan Havránek, Michal Španko and 9 more

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 19 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

19 authors at 5 institutions in 2 countries.

Štepán NovákInstitute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Michal KolářLaboratory of Genomics and Bioinformatics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Arpád SzabóDepartment of Pathology, Third Faculty of Medicine, Charles University and University Hospital Královske Vinohrady, Prague, Czech Republic.
Zdena VernerováDepartment of Pathology, Third Faculty of Medicine, Charles University and University Hospital Královske Vinohrady, Prague, Czech Republic.
Lukáš LacinaInstitute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Hynek StrnadLaboratory of Genomics and Bioinformatics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Jana ŠáchováLaboratory of Genomics and Bioinformatics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Miluše HradilováLaboratory of Genomics and Bioinformatics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Jan HavránekLaboratory of Genomics and Bioinformatics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Michal ŠpankoInstitute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Matúš ČomaDepartment of Pharmacology, Pavol Jozef Šafárik University, Košice, Slovak Republic.
Lukáš UrbanDepartment of Biomedical Research, East-Slovak Institute of Cardiovascular Diseases, Košice, Slovak Republic.
Miriam KaňuchováLaboratory of Cell Interactions, Center of Clinical and Preclinical Research MediPark, Pavol Jozef Šafárik University, Košice, Slovak Republic.
Nikola MelegováLaboratory of Cell Interactions, Center of Clinical and Preclinical Research MediPark, Pavol Jozef Šafárik University, Košice, Slovak Republic.
Robert GürlichDepartment of Surgery, Third Faculty of Medicine, Charles University and University Hospital Královske Vinohrady, Prague, Czech Republic.
Josef DvořákDepartment of Oncology, First Faculty of Medicine, Charles University and Thomayer Hospital, Prague, Czech Republic.
Karel SmetanaInstitute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Peter GálDepartment of Biomedical Research, East-Slovak Institute of Cardiovascular Diseases, Košice, Slovak Republic; pavol.szabo@lf1.cuni.cz pgal@vusch.sk galovci@yahoo.com.
Pavol SzaboInstitute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic; pavol.szabo@lf1.cuni.cz pgal@vusch.sk galovci@yahoo.com.
Charles University · CZCzech Academy of Sciences, Institute of Molecular Genetics · CZUniversity of Pavol Jozef Šafárik · SKUniversity Hospital Kralovske Vinohrady · CZUniversity of Chemistry and Technology, Prague · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimPancreatic ductal adenocarcinoma (PDAC) still represents one of the most aggressive cancers. Understanding of the epithelial-mesenchymal crosstalk as a crucial part of the tumor microenvironment should pave the way for therapies to improve patient survival rates. Well-established cell lines present a useful and reproducible model to study PDAC biology. However, the tumor-stromal interactions between cancer cells and cancer-associated fibroblasts (CAFs) are still poorly understood. MATERIALS AND

methodsWe studied interactions between four PDAC cell lines (Panc-1, CAPAN-2, MIAPaCa-2, and PaTu-8902) and conditioned media derived from primary cultures of normal fibroblasts/PDAC-derived CAFs (PANFs).

resultsWhen the tested PDAC cell lines were stimulated by PANF-derived conditioned media, the most aggressive behavior was acquired by the Panc-1 cell line (increased number and size of colonies, remaining expression of vimentin and keratin 8 as well as increase of epithelial-to-mesenchymal polarization markers), whereas PaTu-8902 cells were rather inhibited. Of note, administration of the conditioned media to MIAPaCa-2 cells resulted in an inverse effect on the size and number of colonies, whereas CAPAN-2 cells were rather stimulated. To explain the heterogeneous pattern of the observed PDAC crosstalk at the in vitro level, we further compared the phenotype of primary cultures of cells derived from ascitic fluid with that of the tested PDAC cell lines, analyzed tumor samples of PDAC patients, and performed gene expression profiling of PANFs. Immuno-cyto/histo-chemical analysis found specific phenotype differences within the group of examined patients and tested PDAC cell lines, whereas the genomic approach in PANFs found the key molecules (IL6, IL8, MFGE8 and periostin) that may contribute to the cancer aggressive behavior.

conclusionThe desmoplastic patient-specific regulation of cancer cells by CAFs (also demonstrated by the heterogeneous response of PDAC cell lines to fibroblasts) precludes simple targeting and development of an effective treatment strategy and rather requires establishment of an individualized tumor-specific treatment protocol.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Pancreatic DuctalCell Line, TumorEpithelial-Mesenchymal TransitionFibroblastsHumansPancreatic NeoplasmsTumor Microenvironmentcancer stem cellEpithelial–mesenchymal interactionpancreastumor micro - environmenttumor stroma

Identifiers

PMID33893076
PMCPMC8126325
OpenAlexW3155718864

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.