Evidence map›Paper›PMID 34001947›Full record

ArticleScientific reports2021

Identification of targets of JS-K against HBV-positive human hepatocellular carcinoma HepG2.2.15 cells with iTRAQ proteomics.

Zhengyun Liu, Yan Xu, Wanling Zhang, Xinghong Gao, Guo Luo, Hong Song, Jie Liu, Huan Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 31 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

8 authors at 1 institution in 1 country.

Zhengyun Liu *Key Laboratory of Infectious Disease and Biosafety, Provincial Department of Education, Guizhou, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Yan Xu *Key Laboratory of Infectious Disease and Biosafety, Provincial Department of Education, Guizhou, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Wanling ZhangDepartment of Microbiology, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Xinghong GaoKey Laboratory of Infectious Disease and Biosafety, Provincial Department of Education, Guizhou, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Guo LuoKey Laboratory of Infectious Disease and Biosafety, Provincial Department of Education, Guizhou, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Hong SongDepartment of Microbiology, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Jie LiuKey Lab for Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine, Zunyi Medical University, Zunyi, 563000, Guizhou, China.
Huan WangKey Laboratory of Infectious Disease and Biosafety, Provincial Department of Education, Guizhou, Zunyi Medical University, Zunyi, 563000, Guizhou, China. wanghuan928@163.com.
Zunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

JS-K, a nitric oxide-releasing diazeniumdiolates, is effective against various tumors. We have discovered that JS-K was effective against Hepatitis B virus (HBV)-positive HepG2.2.15 cells. This study used iTRAQ to identify differentially expressed proteins following JS-K treatment of HepG2.2.15 cells. Silenced Transgelin (shTAGLN-2.15) cells were constructed, and the cell viability was analyzed by the CCK8 assay after treatment with JS-K. There were 182 differentially expressed proteins in JS-K treated-HepG2.2.15 cells; 73 proteins were up-regulated and 109 proteins were down-regulated. These proteins were categorized according to GO classification. KEGG enrichment analysis showed that Endocytosis, Phagosome and Proteoglycans were the most significant pathways. RT-PCR confirmed that the expression levels of TAGLN, IGFBP1, SMTN, SERPINE1, ANXA3, TMSB10, LGALS1 and KRT19 were significantly up-regulated, and the expression levels of C5, RBP4, CHKA, SIRT5 and TRIM14 were significantly down-regulated in JS-K treated-HepG2.2.15 cells. Western blotting confirmed the increased levels of USP13 and TAGLN proteins in JS-K treated-HepG2.2.15 cells. Molecular docking revealed the binding of JS-K to TAGLN and shTAGLN-2.15 cells were resistant to JS-K cytotoxicity, suggesting that TAGLN could be an important target in JS-K anti-HBV-positive liver cancer cells. These proteomic findings could shed new insights into mechanisms underlying the effect of JS-K against HBV-related HCC.

Indexed as

ApoptosisAzo CompoundsCarcinoma, HepatocellularCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticGene SilencingHepatitis BHepatitis B virusHep G2 CellsHumansLiver NeoplasmsMicrofilament ProteinsMolecular Docking SimulationMuscle ProteinsNeoplasm ProteinsAzo CompoundsdiazeniumdiolateMicrofilament ProteinsMuscle ProteinsNeoplasm ProteinsO(2)-(2,4-dinitrophenyl) 1-((4-ethoxycarbonyl)piperazin-1-yl)diazen-1-ium-1,2-diolatePiperazinesProteometransgelinUbiquitin-Specific ProteasesUSP13 protein, human

Identifiers

PMID34001947
PMCPMC8129129
OpenAlexW3163092860

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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.