Evidence map›Paper›PMID 35732625›Full record

ArticleCell death & disease2022

Proteomic analysis reveals USP7 as a novel regulator of palmitic acid-induced hepatocellular carcinoma cell death.

Sandhini Saha, Rohit Verma, Chandan Kumar, Bhoj Kumar, Amit Kumar Dey, Milan Surjit, Sivaram V S Mylavarapu, Tushar Kanti Maiti

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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  11. A Combination of Four Nuclear Targeted Effectors ProtectsbioRxiv : the preprint server for biology · 2023
    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

8 authors at 2 institutions in 1 country.

Sandhini SahaFunctional Proteomics Laboratory, Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad, 121001, India.
Rohit VermaVirology Laboratory, Translational Health Science and Technology Institute, NCR Biotech Science Cluster, Faridabad, 121001, India.
Chandan KumarLaboratory of Cellular Dynamics, Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad, 121001, India.
Bhoj KumarFunctional Proteomics Laboratory, Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad, 121001, India.
Amit Kumar DeyFunctional Proteomics Laboratory, Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad, 121001, India.
Milan SurjitVirology Laboratory, Translational Health Science and Technology Institute, NCR Biotech Science Cluster, Faridabad, 121001, India.
Sivaram V S MylavarapuLaboratory of Cellular Dynamics, Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad, 121001, India.
Tushar Kanti MaitiFunctional Proteomics Laboratory, Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad, 121001, India. tkmaiti@rcb.res.in.ORCID 0000-0003-4721-827X
Regional Centre for Biotechnology · INTranslational Health Science and Technology Institute · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nutrient surplus and consequent free fatty acid accumulation in the liver cause hepatosteatosis. The exposure of free fatty acids to cultured hepatocyte and hepatocellular carcinoma cell lines induces cellular stress, organelle adaptation, and subsequent cell death. Despite many studies, the mechanism associated with lipotoxicity and subsequent cell death still remains poorly understood. Here, we have used the proteomics approach to circumvent the mechanism for lipotoxicity using hepatocellular carcinoma cells as a model. Our quantitative proteomics data revealed that ectopic lipids accumulation in cells severely affects the ubiquitin-proteasomal system. The palmitic acid (PA) partially lowered the expression of deubiquitinating enzyme USP7 which subsequently destabilizes p53 and promotes mitotic entry of cells. Our global phosphoproteomics analysis also provides strong evidence of an altered cell cycle checkpoint proteins' expression that abrogates early G2/M checkpoints recovery with damaged DNA and induced mitotic catastrophe leading to hepatocyte death. We observe that palmitic acid prefers apoptosis-inducing factor (AIF) mediated cell death by depolarizing mitochondria and translocating AIF to the nucleus. In summary, the present study provides evidence of PA-induced hepatocellular death mediated by deubiquitinase USP7 downregulation and subsequent mitotic catastrophe.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsUbiquitin-Specific Peptidase 7ApoptosisCell DeathCell LineHumansPalmitic AcidProteomicsPalmitic AcidUbiquitin-Specific Peptidase 7USP7 protein, human

Identifiers

PMID35732625
PMCPMC9217975
OpenAlexW4283269200

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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.