Evidence map›Paper›PMID 28323861›Full record

ArticlePloS one2017

Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines.

Yuki Haga, Tatsuo Kanda, Masato Nakamura, Shingo Nakamoto, Reina Sasaki, Koji Takahashi, Shuang Wu, Osamu Yokosuka

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-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

26 citing papers in PubMed, 51 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

8 authors at 1 institution in 1 country.

Yuki HagaDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Tatsuo KandaDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.ORCID http://orcid.org/0000-0003-4672-9289
Masato NakamuraDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Shingo NakamotoDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Reina SasakiDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Koji TakahashiDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Shuang WuDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Osamu YokosukaDepartment of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Chiba, Japan.
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite recent advances in treatment strategies, it is still difficult to cure patients with hepatocellular carcinoma (HCC). Sorafenib is the only approved multiple kinase inhibitor for systemic chemotherapy in patients with advanced HCC. The majority of advanced HCC patients are resistant to sorafenib. The mechanisms of sorafenib resistance are still unknown.

methodsThe expression of molecules involved in the mitogen-activated protein kinase (MAPK) signaling pathway in human hepatoma cell lines was examined in the presence or absence of sorafenib. Apoptosis of human hepatoma cells treated with sorafenib was investigated, and the expression of Jun proto-oncogene (c-Jun) was measured.

resultsThe expression and phosphorylation of c-Jun were enhanced in human hepatoma cell lines after treatment with sorafenib. Inhibiting c-Jun enhanced sorafenib-induced apoptosis. The overexpression of c-Jun impaired sorafenib-induced apoptosis. The expression of osteopontin, one of the established AP-1 target genes, was enhanced after treatment with sorafenib in human hepatoma cell lines.

conclusionsThe protein c-Jun plays a role in sorafenib resistance in human hepatoma cell lines. The modulation and phosphorylation of c-Jun could be a new therapeutic option for enhancing responsiveness to sorafenib. Modulating c-Jun may be useful for certain HCC patients with sorafenib resistance.

Indexed as

AnthracenesAntineoplastic AgentsApoptosisCarcinoma, HepatocellularCaspase 3Caspase 7Cell Line, TumorDrug Resistance, NeoplasmHep G2 CellsHumansJNK Mitogen-Activated Protein KinasesLiver NeoplasmsNiacinamideOsteopontinPhenylurea CompoundsPhosphorylationAnthracenesAntineoplastic AgentsCaspase 3Caspase 7JNK Mitogen-Activated Protein KinasesMAS1 protein, humanNiacinamideOsteopontinPhenylurea CompoundsProto-Oncogene MaspyrazolanthroneRNA, Small InterferingSorafenib

Identifiers

PMID28323861
PMCPMC5360329
OpenAlexW2603218477

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.