Evidence map›Paper›PMID 33099479›Full record

ArticleCancer genomics & proteomics

Gigantol Targets MYC for Ubiquitin-proteasomal Degradation and Suppresses Lung Cancer Cell Growth.

Nattanan Losuwannarak, Sittiruk Roytrakul, Pithi Chanvorachote

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

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  8. Integrated analysis ofFrontiers in pharmacology · 2023
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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

3 authors at 2 institutions in 1 country.

Nattanan LosuwannarakCell-Based Drug and Health Product Development Research Unit, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
Sittiruk RoytrakulFunctional Ingredients and Food Innovation Research Group, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathumthani, Thailand.
Pithi ChanvorachoteCell-Based Drug and Health Product Development Research Unit, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand pithi_chan@yahoo.com.
Chulalongkorn University · THNational Center for Genetic Engineering and Biotechnology · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGigantol is a pharmacologically active bibenzyl compound exerting potential anticancer activities. At non-toxic concentrations, it reduces cancer stem cell properties and tumorigenicity. The mechanisms of the effects of gigantol on cancer cell growth are largely unknown. This study aimed to unravel the molecular profile and identify the prominent molecular mechanism of the effects of gigantol in controlling lung cancer cell proliferation. MATERIALS AND

methodsProteomics and bioinformatics analysis were used accompanied by experimental molecular pharmacology approaches.

resultsGigantol exhibited antiproliferative effects on human lung cancer cells confirmed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide proliferation assay and colony growth assay. The protein profile in response to gigantol treatment associated with regulation of cell proliferation was analyzed to determine the prominent protein targets. Among the significant hub proteins, MYC, an important proto-oncogene and proliferation-promoting transcription factor, was down-regulated with the highest number of protein-protein interactions. MYC down-regulation was confirmed by western blot analysis. The up-stream regulator of MYC, Glycogen synthase kinase 3 beta (GSK3β) was found to be responsible for MYC destabilization mediated by gigantol. Gigantol facilitated GSK3β function and resulted in the increase of MYC-ubiquitin complex as evaluated by immunoprecipitation.

conclusionGigantol was found to inhibit lung cancer proliferation through induction of GSK3β-mediated MYC ubiquitin-proteasome degradation. These data suggest gigantol to be a promising candidate for novel strategy in inhibition of lung cancer.

Indexed as

ApoptosisBibenzylsBiomarkers, TumorCell ProliferationGene Expression Regulation, NeoplasticGuaiacolHumansLung NeoplasmsProtein Interaction MapsProtein Processing, Post-TranslationalProteolysisProto-Oncogene MasProto-Oncogene Proteins c-mycTumor Cells, CulturedUbiquitinUbiquitinationBibenzylsBiomarkers, TumorgigantolGuaiacolMAS1 protein, humanMYC protein, humanProto-Oncogene MasProto-Oncogene Proteins c-mycUbiquitincell proliferationDendrobium draconisGigantollung cancerMYCproteomics

Identifiers

PMID33099479
PMCPMC7675646
OpenAlexW3093922735

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.