Evidence map›Paper›PMID 28105937›Full record

ArticleBMC genetics2016

Effect of lentivirus-mediated shRNA inactivation of HK1, HK2, and HK3 genes in colorectal cancer and melanoma cells.

Anna V Kudryavtseva, Maria S Fedorova, Alex Zhavoronkov, Alexey A Moskalev, Alexander S Zasedatelev, Alexey A Dmitriev, Asiya F Sadritdinova, Irina Y Karpova, Kirill M Nyushko, Dmitry V Kalinin and 10 more

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

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  19. Frontiers in genetics · 2020
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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

20 authors at 8 institutions in 2 countries.

Anna V KudryavtsevaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia. rhizamoeba@mail.ru.
Maria S FedorovaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Alex ZhavoronkovInsilico Medicine, Inc., Emerging Technology Centers, Johns Hopkins University Eastern Campus, Baltimore, Maryland, USA.
Alexey A MoskalevEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Alexander S ZasedatelevEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Alexey A DmitrievEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Asiya F SadritdinovaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Irina Y KarpovaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Kirill M NyushkoNational Medical Research Radiological Center, Ministry of Health of the Russian Federation, Moscow, Russia.
Dmitry V KalininA.V. Vishnevsky Institute of Surgery, Moscow, Russia.
Nadezhda N VolchenkoNational Medical Research Radiological Center, Ministry of Health of the Russian Federation, Moscow, Russia.
Nataliya V MelnikovaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Kseniya M KliminaVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, Russia.
Dmitry V SidorovNational Medical Research Radiological Center, Ministry of Health of the Russian Federation, Moscow, Russia.
Anatoly Y PopovState Hospital №57, Moscow, Russia.
Tatiana V NasedkinaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Andrey D KaprinNational Medical Research Radiological Center, Ministry of Health of the Russian Federation, Moscow, Russia.
Boris Y AlekseevNational Medical Research Radiological Center, Ministry of Health of the Russian Federation, Moscow, Russia.
George S KrasnovEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Anastasiya V SnezhkinaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Engelhardt Institute of Molecular Biology · RUMinistry of Health of the Russian Federation · RUInstitute of Surgery named after A. V. Vishnevskogo · RUJohns Hopkins University · USMoscow City Hospital No 29 · RUMoscow Institute of Physics and Technology · RURussian Cancer Research Center NN Blokhin · RUVavilov Institute of General Genetics · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe switch from oxidative phosphorylation to glycolysis in proliferating cancer cells, even under aerobic conditions, has been shown first in 1926 by Otto Warburg. Today this phenomenon is known as the "Warburg effect" and recognized as a hallmark of cancer. The metabolic shift to glycolysis is associated with the alterations in signaling pathways involved in energy metabolism, including glucose uptake and fermentation, and regulation of mitochondrial functions. Hexokinases (HKs), which catalyze the first step of glycolysis, have been identified to play a role in tumorigenesis of human colorectal cancer (CRC) and melanoma. However, the mechanism of action of HKs in the promotion of tumor growth remains unclear.

resultsThe purpose of the present study was to investigate the effect of silencing of hexokinase genes (HK1, HK2, and HK3) in colorectal cancer (HT-29, SW 480, HCT-15, RKO, and HCT 116) and melanoma (MDA-MB-435S and SK-MEL-28) cell lines using short hairpin RNA (shRNA) lentiviral vectors. shRNA lentiviral plasmid vectors pLSLP-HK1, pLSLP-HK2, and pLSLP-HK3 were constructed and then transfected separately or co-transfected into the cells. HK2 inactivation was associated with increased expression of HK1 in colorectal cancer cell lines pointing to the compensation effect. Simultaneous attenuation of HK1 and HK2 levels led to decreased cell viability. Co-transfection with shRNA vectors against HK1, HK2, and HK3 mRNAs resulted in a rapid cell death via apoptosis.

conclusionsWe have demonstrated that simultaneous inactivation of HK1 and HK2 was sufficient to decrease proliferation and viability of melanoma and colorectal cancer cells. Our results suggest that HK1 and HK2 could be the key therapeutic targets for reducing aerobic glycolysis in examined cancers.

Indexed as

ApoptosisCell Line, TumorCell ProliferationColorectal NeoplasmsGenetic VectorsHexokinaseHumansLentivirusMelanomaRNA InterferenceRNA, MessengerRNA, Small InterferingHexokinaseRNA, MessengerRNA, Small InterferingColorectal cancerGlycolysisHexokinasesMelanomashRNAWarburg effect

Identifiers

PMID28105937
PMCPMC5249010
OpenAlexW2561053798

What OpenQuestion holds

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LicenceCC BY
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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.