Evidence map›Paper›PMID 26758620›Full record

ArticleBMC cancer2016

CD133+ liver cancer stem cells resist interferon-gamma-induced autophagy.

Jian Li, Jin-Na Chen, Ting-Ting Zeng, Fan He, Shu-Peng Chen, Stephanie Ma, Jiong Bi, Xiao-Feng Zhu, Xin-Yuan Guan

Abstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

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  16. Immune evasion by cancer stem cells.Regenerative therapy · 2021
    Review
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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

9 authors.

Jian LiDepartment of Clinical Laboratory, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Room 102, 107 W. Yanjiang Road, Guangzhou, 510120, China. lijian57@mail.sysu.edu.cn.
Jin-Na ChenDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. jinnachan2010@gmail.com.
Ting-Ting ZengState Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 651 Dongfeng Road East, Guangzhou, Guangdong, 510060, PR China. zengtt@sysucc.org.cn.
Fan HeDepartment of Forensic Medicine, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China. hefan2@mail2.sysu.edu.cn.
Shu-Peng ChenState Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 651 Dongfeng Road East, Guangzhou, Guangdong, 510060, PR China. chenshp@sysucc.org.cn.
Stephanie MaDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. stephanie.ma@gmail.com.
Jiong BiDepartment of Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. bijiong2000@hotmail.com.
Xiao-Feng ZhuState Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 651 Dongfeng Road East, Guangzhou, Guangdong, 510060, PR China. zhuxfeng@mail.sysu.edu.cn.
Xin-Yuan GuanState Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 651 Dongfeng Road East, Guangzhou, Guangdong, 510060, PR China. xyguan@hkucc.hku.hk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the most fatal malignancies worldwide, and CD133 is a popular cancer stem cell (CSC) marker for HCC. CD133(+) CSCs have been reported to resist conventional chemo- and radiotherapy, but little is known about their response to immune surveillance. Interferon-gamma (IFN-γ) is one of key cytokines that the immune system produce to eradicate cancer cells, so we investigated the function of IFN-γ on CD133+ HCC CSCs in this study.

methodsThe response of CD133(+) cells to IFN-γ was performed with functional assays (cell proliferation assay and tumor formation in nude mice), flow cytometry, immunofluorescence staining and RNA interference.

resultsWe found that IFN-γ inhibited the proliferation of cell lines with low percentage of CD133(+) cells (wild-type human cells, BEL7402, QGY7701) but it did not affect the proliferation of cell lines with high percentage of CD133(+) cells (wild-type human cells, Huh7, PLC8024) in vivo and in vitro (nude mice). Flow cytometry analysis demonstrated that the percentage of CD133+ cells increased after IFN-γ treatment of low CD133(+) cell lines. Furthermore, IFN-γ induced the autophagy of low CD133(+) cell lines to decrease proliferation.

conclusionCD133(+) HCC CSCs resisted IFN-γ-induced autophagy, which might also be a mechanism through which CSCs resist immune eradication.

Indexed as

AC133 AntigenAnimalsAntigens, CDAutophagyCarcinoma, HepatocellularCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlycoproteinsHumansInterferon-gammaLiver NeoplasmsMiceNeoplastic Stem CellsPeptidesXenograft Model Antitumor AssaysAC133 AntigenAntigens, CDGlycoproteinsInterferon-gammaPeptidesPROM1 protein, humanProm1 protein, mouse

Identifiers

PMID26758620
PMCPMC4711109

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.