Evidence map›Paper›PMID 31641101›Full record

ArticleOncogenesis2019

The protein kinase CK2 contributes to the malignant phenotype of cholangiocarcinoma cells.

Giovanni Di Maira, Alessandra Gentilini, Mirella Pastore, Alessandra Caligiuri, Benedetta Piombanti, Chiara Raggi, Elisabetta Rovida, Monika Lewinska, Jesper B Andersen, Christian Borgo and 4 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 36 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

14 authors at 3 institutions in 3 countries.

Giovanni Di MairaDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy.
Alessandra GentiliniDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy.
Mirella PastoreDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy.
Alessandra CaligiuriDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy.
Benedetta PiombantiDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy.
Chiara RaggiDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy.ORCID http://orcid.org/0000-0003-2473-3535
Elisabetta RovidaDipartimento di Scienze Biomediche Sperimentali e Cliniche, Università di Firenze, Florence, Italy.
Monika LewinskaBiotech Research and Innovation Centre (BRIC), Department of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-5275-992X
Jesper B AndersenBiotech Research and Innovation Centre (BRIC), Department of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-1760-5244
Christian BorgoDipartimento di Scienze Biomediche, Università di Padova, Padua, Italy.ORCID http://orcid.org/0000-0001-9540-8145
Mauro SalviDipartimento di Scienze Biomediche, Università di Padova, Padua, Italy.
Daniele OttavianiDipartimento di Scienze Biomediche, Università di Padova, Padua, Italy.
Maria RuzzeneDipartimento di Scienze Biomediche, Università di Padova, Padua, Italy. maria.ruzzene@unipd.it.
Fabio MarraDipartimento di Medicina Sperimentale e Clinica and Center Denothe, Università di Firenze, Florence, Italy. fabio.marra@unifi.it.ORCID http://orcid.org/0000-0001-8629-0878
University of Florence · ITUniversity of Padua · ITUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is a particularly aggressive hepatobiliary malignancy, for which the molecular mechanisms underlying the malignant phenotype are still poorly understood, and novel and effective therapeutic strategies are limited. The pro-survival protein kinase CK2 is frequently overexpressed in cancer and is receiving increasing interest as an anti-tumor drug target. Its precise role in CCA biology is still largely unknown. Here we show that expression of the CK2α and α' catalytic subunits and of the β regulatory subunit is increased in human CCA samples. Increased expression of CK2 subunits was shown in CCA cell lines compared to non-transformed cholangiocytes. We used chemical inhibition of CK2 and genetic modification by CRISPR/Cas9 to explore the contribution of CK2 to the malignant phenotype of CCA cells. Disruption of CK2 activity results in cell death through apoptosis, reduced invasion and migration potential, and G0/G1 cell cycle arrest. Importantly, CCA cells with a reduced CK2 activity are more sensitive to chemotherapy. Altogether, our results demonstrate that CK2 significantly contributes to increased proliferative potential and augmented growth of CCA cells and indicate the rationale for its targeting as a promising pharmacologic strategy for cholangiocarcinoma.

Identifiers

PMID31641101
PMCPMC6805921
OpenAlexW2981904442

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.