Evidence map›Paper›PMID 31078904›Full record

ArticleThe Journal of nutritional biochemistry2019

Quercetin inhibits growth of hepatocellular carcinoma by apoptosis induction in part via autophagy stimulation in mice.

Yi Ji, Li Li, Yan-Xia Ma, Wen-Ting Li, Liu Li, Heng-Zhou Zhu, Mian-Hua Wu, Jin-Rong Zhou

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
8.8field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 102 citations in OpenAlex.

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  4. [Silybin inhibits fibrosis after glaucoma filtration surgery in rabbits by promoting fibroblast autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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 2 institutions in 2 countries.

Yi JiAffiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China; First Clinical Medical College, Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine Prevention and Treatment of Cancer, Nanjing University of Chinese Medicine, Nanjing, China; Nutrition/Metabolism Laboratory, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Li LiAffiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China; First Clinical Medical College, Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine Prevention and Treatment of Cancer, Nanjing University of Chinese Medicine, Nanjing, China.
Yan-Xia MaCollege of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Wen-Ting LiAffiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China; First Clinical Medical College, Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine Prevention and Treatment of Cancer, Nanjing University of Chinese Medicine, Nanjing, China.
Liu LiFirst Clinical Medical College, Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine Prevention and Treatment of Cancer, Nanjing University of Chinese Medicine, Nanjing, China.
Heng-Zhou ZhuAffiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China; First Clinical Medical College, Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine Prevention and Treatment of Cancer, Nanjing University of Chinese Medicine, Nanjing, China.
Mian-Hua WuAffiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China; First Clinical Medical College, Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine Prevention and Treatment of Cancer, Nanjing University of Chinese Medicine, Nanjing, China. Electronic address: wmh7001@163.com.
Jin-Rong ZhouNutrition/Metabolism Laboratory, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: jrzhou@bidmc.harvard.edu.
Nanjing University of Chinese Medicine · CNBeth Israel Deaconess Medical Center · US

Funding

Synergy between phytochemicals for prostate cancer preventionR03CA130133 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHOU, JIN-RONG · 2007 to 2008
$170k
NCI NIH HHS R03 CA130133
6 · The paper itself

Abstract

Quercetin (QCT) has been shown to have anticancer activities associated with apoptosis and autophagy induction. However, whether autophagy is functionally responsible for the inhibitory effect of QCT on hepatocellular carcinoma (HCC) remains elusive. This study aims to investigate if QCT inhibits HCC growth via autophagy induction. The in vitro experiments showed that QCT inhibited the growth of human HCC cells in dose- and time-dependent manners and had minimal cytotoxicity to normal hepatocytes. QCT increased both autophagosomes and autolysosomes in HCC cells, as determined by electron microscopy, GFP-RFP-LC3 fluorescence confocal microscopy and Western blot analysis of autophagy-related biomarkers. Functional assays using pathway-specific inhibitors, activators or siRNAs indicated that QCT stimulated autophagy in part via inhibiting the AKT/mTOR pathway and activating the MAPK pathways. Further functional experiments using autophagy inhibitors demonstrated that QCT induced apoptosis of HCC cells in part via stimulating autophagy. The in vivo studies showed that QCT significantly inhibited tumor growth associated with apoptosis induction and autophagy stimulation, and that inhibition of autophagy significantly alleviated the QCT effect on tumor growth inhibition and apoptosis induction. To the best of our knowledge, this is the first in vivo report to demonstrate that QCT inhibits HCC tumor growth and induces apoptosis in part via stimulation of autophagy. Our results provide strong experimental evidence to support that autophagy stimulation may be an important mechanism by which QCT induces cancer cell apoptosis, and pave the way for further clinical investigations by applying QCT or QCT-rich foods for HCC intervention.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosisAutophagyCarcinoma, HepatocellularGene Expression Regulation, NeoplasticHepatocytesHep G2 CellsHumansLiver NeoplasmsMaleMice, Inbred BALB CProto-Oncogene Proteins c-aktQuercetinTOR Serine-Threonine KinasesXenograft Model Antitumor AssaysAntineoplastic Agents, PhytogenicMTOR protein, humanProto-Oncogene Proteins c-aktQuercetinTOR Serine-Threonine KinasesAKT/mTORApoptosisAutophagyHepatocellular carcinomaMAPKQuercetin

Identifiers

PMID31078904
PMCPMC9659433
OpenAlexW2940007769

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.