Evidence map›Paper›PMID 30186163›Full record

ArticleFrontiers in pharmacology2018

Inhibition of Chloride Intracellular Channel 1 (CLIC1) as Biguanide Class-Effect to Impair Human Glioblastoma Stem Cell Viability.

Federica Barbieri, Roberto Würth, Alessandra Pattarozzi, Ivan Verduci, Chiara Mazzola, Maria G Cattaneo, Michele Tonelli, Agnese Solari, Adriana Bajetto, Antonio Daga and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. 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
1.8field-weighted citation impact, top 15% 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, 43 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

13 authors at 3 institutions in 1 country.

Federica BarbieriSezione di Farmacologia, Dipartimento di Medicina Interna and Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy.
Roberto WürthSezione di Farmacologia, Dipartimento di Medicina Interna and Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy.
Alessandra PattarozziSezione di Farmacologia, Dipartimento di Medicina Interna and Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy.
Ivan VerduciDipartimento di Bioscienze, Università degli Studi di Milano, Milan, Italy.
Chiara MazzolaDipartimento di Bioscienze, Università degli Studi di Milano, Milan, Italy.
Maria G CattaneoDipartimento di Biotecnologie Mediche e Medicina Traslazionale, Università degli Studi di Milano, Milan, Italy.
Michele TonelliDipartimento di Farmacia, Università di Genova, Genova, Italy.
Agnese SolariSezione di Farmacologia, Dipartimento di Medicina Interna and Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy.
Adriana BajettoSezione di Farmacologia, Dipartimento di Medicina Interna and Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy.
Antonio DagaIRCCS, Ospedale Policlinico San Martino, Genova, Italy.
Lucia M VicentiniDipartimento di Biotecnologie Mediche e Medicina Traslazionale, Università degli Studi di Milano, Milan, Italy.
Michele MazzantiDipartimento di Bioscienze, Università degli Studi di Milano, Milan, Italy.
Tullio FlorioSezione di Farmacologia, Dipartimento di Medicina Interna and Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy.
University of Genoa · ITUniversity of Milan · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antidiabetic biguanide metformin exerts antiproliferative effects in different solid tumors. However, during preclinical studies, metformin concentrations required to induce cell growth arrest were invariably within the mM range, thus difficult to translate in a clinical setting. Consequently, the search for more potent metformin derivatives is a current goal for new drug development. Although several cell-specific intracellular mechanisms contribute to the anti-tumor activity of metformin, the inhibition of the chloride intracellular channel 1 activity (CLIC1) at G1/S transition is a key events in metformin antiproliferative effect in glioblastoma stem cells (GSCs). Here we tested several known biguanide-related drugs for the ability to affect glioblastoma (but not normal) stem cell viability, and in particular: phenformin, a withdrawn antidiabetic drug; moroxydine, a former antiviral agent; and proguanil, an antimalarial compound, all of them possessing a linear biguanide structure as metformin; moreover, we evaluated cycloguanil, the active form of proguanil, characterized by a cyclized biguanide moiety. All these drugs caused a significant impairment of GSC proliferation, invasiveness, and self-renewal reaching IC

Indexed as

biguanidescancer stem cellsCLIC1glioblastomametforminproliferation

Identifiers

PMID30186163
PMCPMC6110922
OpenAlexW2888000792

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.