Evidence map›Paper›PMID 29484365›Full record

ArticleInternational journal of molecular medicine2018

LicA induces autophagy through ULK1/Atg13 and ROS pathway in human hepatocellular carcinoma cells.

Qiang Niu, Wei Zhao, Jin Wang, Chunming Li, Tao Yan, Wei Lv, Guojing Wang, Weihong Duan, Tao Zhang, Kunnan Wang and 1 more

Abstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Review
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  5. Review
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  7. Article
  8. Review
  9. Licorice (OncoTargets and therapy · 2022
    Review
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  13. 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

11 authors.

Qiang NiuDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Wei ZhaoDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Jin WangDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Chunming LiDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Tao YanDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Wei LvDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Guojing WangDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Weihong DuanDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Tao ZhangDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Kunnan WangDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.
Dinghua ZhouDepartment of Hepatobiliary Surgery, Rocket Army General Hospital, Beijing 100088, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy is the best choice for the vast majority of hepatocellular carcinoma patients at late stage, but few effective chemotherapy drugs are available in clinic. Licochalcone A (LicA) is a new chemotherapy drug inducing apoptosis as Bcl-2 inhibitor, but few studies report on LicA‑induced autophagy. This study investigated the phenomenon and mechanisms of LicA-induced autophagy looking for a targeted combination drug. Human hepatocellular carcinoma cells (HCCs) were treated with LicA, to detect markers of autophagy and to investigate the mechanisms. In order to investigate the role of reactive oxygen species (ROS) in LicA‑induced autophagy, ROS, glutathione (GSH) and O2- were measured in LicA treated HCCs, and antioxidant N-Acetyl-L-cysteine (NAC) was cotreated with LicA in HCCs, then mechanisms of ROS-induced autophagy was investigated in LicA or LicA combined with NAC treated HCCs. Finally, the LicA-induced apoptosis was detected in LicA combined with NAC treated HCCs. We first report that LicA can induce autophagy through ULK1/Atg13 and ROS pathway in HCCs, suppression of LicA-induced ROS through antioxidant NAC can enhance LicA-induced apoptosis, promoting the function of LicA killing HCCs. LicA can activate the ULK1/Atg13 complex which is upstream of autophagy, additionally, LicA also can promote ROS generation, ROS trigger the expression level of TSC1/2 complex, PRAS40, CTMP, PP2A, PDK1 and Rubicon change, these molecules are upstream of autophagy. In conclusion, LicA can induce autophagy through ULK1/Atg13 and ROS pathway in HCCs, LicA combined with NAC can enhance LicA-induced apoptosis. Our results may provide a novel design for clinical hepatocellular carcinoma therapy trials.

Indexed as

Adaptor Proteins, Signal TransducingAntineoplastic Agents, PhytogenicAutophagyAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsCarcinoma, HepatocellularCell Line, TumorChalconesHep G2 CellsHumansIntracellular Signaling Peptides and ProteinsLiver NeoplasmsReactive Oxygen SpeciesSignal TransductionAdaptor Proteins, Signal TransducingAntineoplastic Agents, PhytogenicATG13 protein, humanAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsChalconesIntracellular Signaling Peptides and Proteinslicochalcone AReactive Oxygen SpeciesULK1 protein, human

Identifiers

PMID29484365
PMCPMC5846666

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.