Evidence map›Paper›PMID 36050738›Full record

ArticleCell communication and signaling : CCS2022

Apoptin mediates mitophagy and endogenous apoptosis by regulating the level of ROS in hepatocellular carcinoma.

Yiquan Li, Chao Shang, Zirui Liu, Jicheng Han, Wenjie Li, Pengpeng Xiao, Nan Li, Shanzhi Li, Zhiru Xiu, Gaojie Song and 5 more

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 34 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

15 authors at 4 institutions in 1 country.

Yiquan Li *Academician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.ORCID 0000-0002-6795-6088
Chao Shang *Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
Zirui Liu *Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, 130122, People's Republic of China.
Jicheng HanAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.
Wenjie LiInstitute of Virology, Wenzhou University, Wenzhou, 325035, People's Republic of China.
Pengpeng XiaoInstitute of Virology, Wenzhou University, Wenzhou, 325035, People's Republic of China.
Nan LiInstitute of Virology, Wenzhou University, Wenzhou, 325035, People's Republic of China.
Shanzhi LiAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.
Zhiru XiuAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.
Gaojie SongAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.
Yaru LiAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.
Ningyi JinAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China.
Jinbo FangAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China. fangjb792@yahoo.com.
Xiao LiAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China. skylee6226@163.com.
Yilong ZhuAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, No. 1035, Boshuo Road, Jingyue Economic and Technological Development Zone, Changchun, 130117, Jilin, People's Republic of China. 362976499@qq.com.
Changchun University of Chinese Medicine · CNWenzhou University · CNChinese Academy of Agricultural Sciences · CNChangchun Institute of Applied Chemistry · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApoptin, as a tumor-specific pro-apoptotic protein, plays an important anti-tumoral role, but its mechanism of autophagy activation and the interaction between autophagy and apoptosis have not been accurately elucidated. Here, we studied the mechanism of apoptin-induced apoptosis and autophagy and the interaction between two processes.

methodsUsing crystal violet staining and the CCK-8 assay, we analyzed the effect of apoptin in the inhibition of liver cancer cells in vitro and analyzed the effect of inhibiting liver cancer in vivo by establishing a nude mouse tumor model. Flow cytometry and fluorescence staining were used to analyze the main types of apoptin-induced apoptosis and autophagy. Subsequently, the relationship between the two events was also analyzed. Flow cytometry was used to analyze the effect of ROS on apoptin-mediated apoptosis and autophagy mediated by apoptin. The effect of ROS on two phenomena was analyzed. Finally, the role of key genes involved in autophagy was analyzed using gene silencing.

resultsThe results showed that apoptin can significantly increase the apoptosis and autophagy of liver cancer cells, and that apoptin can cause mitophagy through the increase in the expression of NIX protein. Apoptin can also significantly increase the level of cellular ROS, involved in apoptin-mediated autophagy and apoptosis of liver cancer cells. The change of ROS may be a key factor causing apoptosis and autophagy.

conclusionThe above results indicate that the increase in ROS levels after apoptin treatment of liver cancer cells leads to the loss of mitochondrial transmembrane potential, resulting in endogenous apoptosis and mitophagy through the recruitment of NIX. Therefore, ROS may be a key factor connecting endogenous apoptosis and autophagy induced by apoptin in liver cancer cells. Video abstract.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsApoptosisCapsid ProteinsMiceMice, NudeMitophagyReactive Oxygen SpeciesCapsid ProteinsReactive Oxygen SpeciesApoptinApoptosisAutophagyHuman liver cancerROS

Identifiers

PMID36050738
PMCPMC9438158
OpenAlexW4294024949

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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.