Evidence map›Paper›PMID 32466311›Full record

ArticleInternational journal of molecular sciences2020

Dual Targeting of Stromal Cell Support and Leukemic Cell Growth by a Peptidic PKC Inhibitor Shows Effectiveness against B-ALL.

Paola Fernanda Ruiz-Aparicio, Natalia-Del Pilar Vanegas, Gloria Inés Uribe, Paola Ortiz-Montero, Camila Cadavid-Cortés, Jimmy Lagos, Jessica Flechas-Afanador, Adriana Linares-Ballesteros, Jean-Paul Vernot

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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 15 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

9 authors at 1 institution in 1 country.

Paola Fernanda Ruiz-AparicioGrupo de Investigación Fisiología Celular y Molecular, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá D. C. 111321, Colombia.ORCID 0000-0002-8486-9883
Natalia-Del Pilar VanegasGrupo de Investigación Fisiología Celular y Molecular, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá D. C. 111321, Colombia.ORCID 0000-0001-5135-1714
Gloria Inés UribeGrupo de Investigación Oncohematología Pediátrica, Fundación Hospital de la Misericordia, Universidad Nacional de Colombia, Bogotá D. C. 111071, Colombia.
Paola Ortiz-MonteroGrupo de Investigación Fisiología Celular y Molecular, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá D. C. 111321, Colombia.
Camila Cadavid-CortésGrupo de Investigación Fisiología Celular y Molecular, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá D. C. 111321, Colombia.
Jimmy LagosGrupo de Investigación Oncohematología Pediátrica, Fundación Hospital de la Misericordia, Universidad Nacional de Colombia, Bogotá D. C. 111071, Colombia.
Jessica Flechas-AfanadorGrupo de Investigación Oncohematología Pediátrica, Fundación Hospital de la Misericordia, Universidad Nacional de Colombia, Bogotá D. C. 111071, Colombia.
Adriana Linares-BallesterosGrupo de Investigación Oncohematología Pediátrica, Fundación Hospital de la Misericordia, Universidad Nacional de Colombia, Bogotá D. C. 111071, Colombia.
Jean-Paul VernotGrupo de Investigación Fisiología Celular y Molecular, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá D. C. 111321, Colombia.ORCID 0000-0002-0237-3375
Universidad Nacional de Colombia · CO

Funding

Departamento Administrativo de Ciencia, Tecnología e Innovación (COLCIENCIAS) 58257Facultad de Medicina, Universidad Nacional de Colombia 40181
6 · The paper itself

Abstract

Mesenchymal stem cells (MSC) favour a scenario where leukemic cells survive. The protein kinase C (PKC) is essential to confer MSC support to leukemic cells and may be responsible for the intrinsic leukemic cell growth. Here we have evaluated the capacity of a chimeric peptide (HKPS), directed against classical PKC isoforms, to inhibit leukemic cell growth. HKPS was able to strongly inhibit viability of different leukemic cell lines, while control HK and PS peptides had no effect. Further testing showed that 30% of primary samples from paediatric B-cell acute lymphoblastic leukaemia (B-ALL) were also strongly affected by HKPS. We showed that HKPS disrupted the supportive effect of MSC that promote leukemic cell survival. Interestingly, ICAM-1 and VLA-5 expression increased in MSC during the co-cultures with B-ALL cells, and we found that HKPS inhibited the interaction between MSC and B-ALL cells due to a reduction in the expression of these adhesion molecules. Of note, the susceptibility of B-ALL cells to dexamethasone increased when MSC were treated with HKPS. These results show the relevance of these molecular interactions in the leukemic niche. The use of HKPS may be a new strategy to disrupt intercellular communications, increasing susceptibility to therapy, and at the same time, directly affecting the growth of PKC-dependent leukemic cells.

Indexed as

Antineoplastic AgentsB-LymphocytesCell AdhesionCell ProliferationCells, CulturedChildEnzyme InhibitorsHumansIntegrinsIntercellular Adhesion Molecule-1Jurkat CellsK562 CellsMesenchymal Stem CellsOligopeptidesPrecursor Cell Lymphoblastic Leukemia-LymphomaProtein Kinase CAntineoplastic AgentsEnzyme InhibitorsIntegrinsIntercellular Adhesion Molecule-1OligopeptidesProtein Kinase CRecombinant ProteinsB-ALLcell adhesionchimeric peptideleukemic microenvironmentmesenchymal supportPKC

Identifiers

PMID32466311
PMCPMC7279155
OpenAlexW3027924039

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.