Evidence map›Paper›PMID 31979110›Full record

ArticleInternational journal of molecular sciences2020

Analysis of the Effect of Increased α2,3-Sialylation on RTK Activation in MKN45 Gastric Cancer Spheroids Treated with Crizotinib.

Meritxell Balmaña, Francisca Diniz, Tália Feijão, Cristina C Barrias, Stefan Mereiter, Celso A Reis

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. 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 23% 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, 26 citations in OpenAlex.

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  9. A roadmap for translational cancer glycoimmunology at single cell resolution.Journal of experimental & clinical cancer research : CR · 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

6 authors at 1 institution in 1 country.

Meritxell Balmañai3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
Francisca Dinizi3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
Tália Feijãoi3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
Cristina C Barriasi3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
Stefan Mereiteri3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
Celso A Reisi3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
Universidade do Porto · PT

Funding

European Regional Development Fund NORTE-01-0145-FEDER-000029European Regional Development Fund POCI-01-0145-FEDER-007274European Regional Development Fund POCI-01-0145-FEDER-016585Fundação para a Ciência e a Tecnologia CEECIND/02760/2017Fundação para a Ciência e a Tecnologia IF/00296/2015Fundação para a Ciência e a Tecnologia PTDC/BBB-EBI/0567/2014Fundação para a Ciência e a Tecnologia PTDC/BBB-ECT/2518/2014Fundação para a Ciência e a Tecnologia SFRH/BD/137896/2018H2020 Marie Skłodowska-Curie Actions 748880
6 · The paper itself

Abstract

In the scenario of personalized medicine, targeted therapies are currently the focus of cancer drug development. These drugs can block the growth and spread of tumor cells by interfering with key molecules involved in malignancy, such as receptor tyrosine kinases (RTKs). MET and Recepteur d'Origine Nantais (RON), which are RTKs frequently overactivated in gastric cancer, are glycoprotein receptors whose activation have been shown to be modulated by the cellular glycosylation. In this work, we address the role of sialylation in gastric cancer therapy using an innovative 3D high-throughput cell culture methodology that mimics better the in vivo tumor features. We evaluate the response to targeted treatment of glycoengineered gastric cancer cell models overexpressing the sialyltransferases ST3GAL4 or ST3GAL6 by subjecting 3D spheroids to the tyrosine kinase inhibitor crizotinib. We show here that 3D spheroids of ST3GAL4 or ST3GAL6 overexpressing MKN45 gastric cancer cells are less affected by the inhibitor. In addition, we disclose a potential compensatory pathway via activation of the Insulin Receptor upon crizotinib treatment. Our results suggest that cell sialylation, in addition of being involved in tumor progression, could play a critical role in the response to tyrosine kinase inhibitors in gastric cancer.

Indexed as

Antineoplastic AgentsCell Line, TumorCrizotinibHumansProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesRNA, Small InterferingSialyltransferasesStomach NeoplasmsAntineoplastic AgentsCrizotinibProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesRNA, Small InterferingSialyltransferases3D cell culturecrizotinibgastric cancerglycosylationMETreceptor tyrosine kinaseRONsialylationspheroidstyrosine kinase inhibitor

Identifiers

PMID31979110
PMCPMC7037121
OpenAlexW3002211575

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.