Evidence map›Paper›PMID 31632072›Full record

ArticleOncoTargets and therapy2019

The Roles Of Angiogenesis And Cancer Stem Cells In Sorafenib Drug Resistance In Hepatocellular Carcinoma.

Chiung-Chi Cheng, Wei-Ting Chao, Chen-Chun Liao, Jing-Hao Shih, Yih-Shyong Lai, Yung-Hsiang Hsu, Yi-Hsiang Liu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  6. Microvesicles: the functional mediators in sorafenib resistance.Cancer drug resistance (Alhambra, Calif.) · 2022
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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 4 institutions in 1 country.

Chiung-Chi ChengDepartment of Pathology, Chang Bing Show-Chwan Memorial Hospital, Changhua 505, Taiwan.
Wei-Ting ChaoDepartment of Life Science, Tunghai University, Taichung City 407, Taiwan.
Chen-Chun LiaoDepartment of Life Science, Tunghai University, Taichung City 407, Taiwan.
Jing-Hao ShihDepartment of Life Science, Tunghai University, Taichung City 407, Taiwan.
Yih-Shyong LaiDepartment of Pathology, Chang Bing Show-Chwan Memorial Hospital, Changhua 505, Taiwan.
Yung-Hsiang HsuDepartment of Pathology, Tzu Chi University, Hualien 97004, Taiwan.
Yi-Hsiang LiuDepartment of Pathology, Chang Bing Show-Chwan Memorial Hospital, Changhua 505, Taiwan.ORCID 0000-0001-5518-2524
Tunghai University · TWTzu Chi University · TWChang Bing Show Chwan Memorial Hospital · TWProvidence University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAn increasing number of studies support cancer stem cells as the reason for chemoresistance to sorafenib therapy in hepatocellular carcinoma (HCC), but the mechanism is still unclear. In this study, the mechanism of sorafenib resistance in cancer stem cells was examined by in vitro experiments and xenograft mouse model.

methodsThe expression of cancer stem cell markers in the Chang liver cell line and PLC/PRF/5 and HepG2 hepatoma cell lines were compared by immunoblot assay before and after sorafenib treatment in vitro. As a xenograft mouse model, subcutaneous injection of hepatoma cells followed by sorafenib therapy was performed in NU/NU mice. The effects of sorafenib therapy on tumor growth and cancer stem cell markers were studied. Angiogenesis associated with cancer stem cells was studied by immunoblot and immunohistochemistry assay.

resultsThe expression of cancer stem cell markers was higher in PLC/PRF/5 and HepG2 cells than Chang liver cells, indicating that these hepatoma cells had more stemness-related characteristics. The cancer stem cell markers were upregulated in the hepatoma cell lines following sorafenib treatment in vitro. In the xenograft model, tumors from PLC/PRF/5 and HepG2 cells with high E-cadherin expression were more resistance to sorafenib therapy. However, the expression of cancer stem cell markers was not significantly different after sorafenib therapy in these tumors. Furthermore, we found that sorafenib therapy induced angiogenesis within tumors from high E-cadherin expressing hepatoma cells.

conclusionThe mechanism of chemoresistance in sorafenib therapy in HCC may be the tumor angiogenesis associated with high E-cadherin expression in cancer stem cells.

Indexed as

angiogenesiscancer stem cellscytokeratinE-cadherinhepatocellular carcinomasorafenib

Identifiers

PMID31632072
PMCPMC6783114
OpenAlexW2977404620

What OpenQuestion holds

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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.