Evidence map›Paper›PMID 22777740›Full record

ArticleJournal of cellular physiology2013

Fluoro-Sorafenib (Regorafenib) effects on hepatoma cells: growth inhibition, quiescence, and recovery.

Brian I Carr, Aldo Cavallini, Catia Lippolis, Rosalba D'Alessandro, Caterina Messa, Maria G Refolo, Angela Tafaro

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
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  5. Deciphering the role of the MALT1-RC3H1 axis in regulating GPX4 protein stability.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
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  8. Selenylated Imidazo [1,2-Pharmaceuticals (Basel, Switzerland) · 2023
    Article
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  18. Regorafenib and ginsenoside combination therapy: inhibition of HepG2 cell growth through modulating survivin and caspase-3 gene expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Article
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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

7 authors at 1 institution in 1 country.

Brian I CarrLaboratory of Biochemistry, National Institute for Digestive Diseases, IRCCS Saverio de Bellis, Castellana Grotte, Italy. brianicarr@hotmail.com
Aldo Cavallini
Catia Lippolis
Rosalba D'Alessandro
Caterina Messa
Maria G Refolo
Angela Tafaro
Gastroenterology Hospital "Saverio de Bellis" · IT

Funding

K VITAMINS--A NEW CLASS OF LIVER CELL GROWTH INHIBITORSR01CA082723 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CARR, BRIAN I · 2000 to 2008
$2.3M
NCI NIH HHS R01 CA082723
6 · The paper itself

Abstract

To evaluate the growth-inhibitory properties of the potent multi-kinase antagonist Regorafenib (Fluoro-Sorafenib), which was synthesized as a more potent Sorafenib, a Raf inhibitor and to determine whether similar mechanisms were involved, human hepatoma cell lines were grown in the presence or absence of Regorafanib and examined for growth inhibition. Western blots were performed for Raf targets, apoptosis, and autophagy. Regorafenib inhibited growth of human Hep3B, PLC/PRF/5, and HepG2 cells in a concentration- and time-dependent manner. Multiple signaling pathways were altered, including MAP kinases phospho-ERK and phospho-JNK and its target phospho-c-Jun. There was evidence for apoptosis by FACS, cleavage of caspases and increased Bax levels; as well as induction of autophagy, as judged by increased Beclin-1 and LC3 (II) levels. Prolonged drug exposure resulted in cell quiescence. Full growth recovery occurred after drug removal, unlike with doxorubicin chemotherapy. Regorafenib is a potent inhibitor of cell growth. Cells surviving Regorafenib treatment remain viable, but quiescent and capable of regrowth following drug removal. The reversibility of tumor cell growth suppression after drug removal may have clinical implications.

Indexed as

Antineoplastic AgentsApoptosisAutophagyCarcinoma, HepatocellularCell Line, TumorCell ProliferationDoxorubicinHumansLiver NeoplasmsPhenylurea CompoundsProtein Kinase InhibitorsPyridinesSignal TransductionAntineoplastic AgentsDoxorubicinPhenylurea CompoundsProtein Kinase InhibitorsPyridinesregorafenib

Identifiers

PMID22777740
PMCPMC4509637
OpenAlexW2111185880

What OpenQuestion holds

Textmetadata
LicenceTDM
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.