Evidence map›Paper›PMID 33723318›Full record

ArticleScientific reports2021

All-trans retinoic acid and protein kinase C α/β1 inhibitor combined treatment targets cancer stem cells and impairs breast tumor progression.

Damian Emilio Berardi, Lizeth Ariza Bareño, Natalia Amigo, Luciana Cañonero, Maria de Las Nieves Pelagatti, Andrea Nora Motter, María Agustina Taruselli, María Inés Díaz Bessone, Stefano Martin Cirigliano, Alexis Edelstein and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

7 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

14 authors at 6 institutions in 2 countries.

Damian Emilio Berardi *Research Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Lizeth Ariza Bareño *Research Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Natalia AmigoResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Luciana CañoneroFacultad de Ciencias Exactas y Naturales, Departamento Química Biológica, Instituto de Química Biológica de la Facultad de Ciencias Exactas Y Naturales (IQUIBICEN), Universidad de Buenos Aires, CONICET-Universidad de Buenos Aires, Buenos Aires, Argentina.
Maria de Las Nieves PelagattiResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Andrea Nora MotterUnidad Operativa Centro de Contención Biológica de la Administracion Nacional de Laboratorios e Institutos de Salud (UOCCB-ANLIS), "Dr. Carlos G. Malbrán", Buenos Aires, Argentina.
María Agustina TaruselliResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
María Inés Díaz BessoneResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Stefano Martin CiriglianoResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Alexis EdelsteinUnidad Operativa Centro de Contención Biológica de la Administracion Nacional de Laboratorios e Institutos de Salud (UOCCB-ANLIS), "Dr. Carlos G. Malbrán", Buenos Aires, Argentina.
María Giselle PetersResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Miriam DiamentResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Alejandro Jorge UrtregerResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina.
Laura Beatriz TodaroResearch Area, Instituto de Oncología "Ángel H. Roffo", Área Investigación, Universidad de Buenos Aires, Av. San Martín 5481, C1417DTB, Buenos Aires, Argentina. ltodaro@gmail.com.
University of Buenos Aires · ARAdministración Nacional de Laboratorios e Institutos de Salud · ARCentro Científico Tecnológico - San Juan · ARCornell University · USNational University of General San Martín · ARUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the leading cause of cancer death among women worldwide. Blocking a single signaling pathway is often an ineffective therapy, especially in the case of aggressive or drug-resistant tumors. Since we have previously described the mechanism involved in the crosstalk between Retinoic Acid system and protein kinase C (PKC) pathway, the rationale of our study was to evaluate the effect of combining all-trans-retinoic acid (ATRA) with a classical PCK inhibitor (Gö6976) in preclinical settings. Employing hormone-independent mammary cancer models, Gö6976 and ATRA combined treatment induced a synergistic reduction in proliferative potential that correlated with an increased apoptosis and RARs modulation towards an anti-oncogenic profile. Combined treatment also impairs growth, self-renewal and clonogenicity potential of cancer stem cells and reduced tumor growth, metastatic spread and cancer stem cells frequency in vivo. An in-silico analysis of "Kaplan-Meier plotter" database indicated that low PKCα together with high RARα mRNA expression is a favorable prognosis factor for hormone-independent breast cancer patients. Here we demonstrate that a classical PKC inhibitor potentiates ATRA antitumor effects also targeting cancer stem cells growth, self-renewal and frequency.

Indexed as

Mammary Neoplasms, ExperimentalNeoplasm ProteinsProtein Kinase C-alphaProtein Kinase C betaAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorFemaleMiceMice, Inbred BALB CNeoplastic Stem CellsProtein Kinase InhibitorsTretinoinNeoplasm ProteinsPrkca protein, mousePrkcb protein, mouseProtein Kinase C-alphaProtein Kinase C betaProtein Kinase InhibitorsTretinoin

Identifiers

PMID33723318
PMCPMC7961031
OpenAlexW3136444002

What OpenQuestion holds

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LicenceCC BY
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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.