Evidence map›Paper›PMID 25586669›Full record

ArticleScientific reports2015

NQO1-induced activation of AMPK contributes to cancer cell death by oxygen-glucose deprivation.

Hyemi Lee, Eun-Taex Oh, Bo-Hwa Choi, Moon-Taek Park, Ja-Kyeong Lee, Jae-Seon Lee, Heon Joo Park

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

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  7. Roles of NADMolecules (Basel, Switzerland) · 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

7 authors at 1 institution in 1 country.

Hyemi LeeDepartment of Microbiology, Inha Research Institute for Medical Sciences, College of Medicine, Inha University, Incheon, Korea.
Eun-Taex Oh1] Department of Microbiology, Inha Research Institute for Medical Sciences, College of Medicine, Inha University, Incheon, Korea [2] Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon, Korea.
Bo-Hwa Choi1] Department of Microbiology, Inha Research Institute for Medical Sciences, College of Medicine, Inha University, Incheon, Korea [2] Pohang Center for Evaluation of Biomaterials, Pohang Technopark, Pohang, Gyeongbuk, Korea.
Moon-Taek Park1] Department of Microbiology, Inha Research Institute for Medical Sciences, College of Medicine, Inha University, Incheon, Korea [2] Research Center, Dongnam Institute of Radiological &Medical Sciences (DIRAMS), Busan, Korea.
Ja-Kyeong Lee1] Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon, Korea [2] Department of Anatomy, College of Medicine, Inha University, Incheon, Korea.
Jae-Seon Lee1] Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon, Korea [2] Department of Biomedical Sciences, College of Medicine, Inha University, Incheon, Korea.
Heon Joo Park1] Department of Microbiology, Inha Research Institute for Medical Sciences, College of Medicine, Inha University, Incheon, Korea [2] Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon, Korea.
Inha University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxygen and glucose deprivation (OGD) due to insufficient blood circulation can decrease cancer cell survival and proliferation in solid tumors. OGD increases the intracellular [AMP]/[ATP] ratio, thereby activating the AMPK. In this study, we have investigated the involvement of NQO1 in OGD-mediated AMPK activation and cancer cell death. We found that OGD activates AMPK in an NQO1-dependent manner, suppressing the mTOR/S6K/4E-BP1 pathway, which is known to control cell survival. Thus, the depletion of NQO1 prevents AMPK-induced cancer cell death in OGD. When we blocked OGD-induced Ca(2+)/CaMKII signaling, the NQO1-induced activation of AMPK was attenuated. In addition, when we blocked the RyR signaling, the accumulation of intracellular Ca(2+) and subsequent activation of CaMKII/AMPK signaling was decreased in NQO1-expressing cells under OGD. Finally, siRNA-mediated knockdown of CD38 abrogated the OGD-induced activation of Ca(2+)/CaMKII/AMPK signaling. Taken together, we conclude that NQO1 plays a key role in the AMPK-induced cancer cell death in OGD through the CD38/cADPR/RyR/Ca(2+)/CaMKII signaling pathway.

Indexed as

ADP-ribosyl Cyclase 1AMP-Activated Protein KinasesAnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channel BlockersCalcium SignalingCell DeathCell Line, TumorCyclic ADP-RiboseEnzyme ActivationGlucoseHumansMiceModels, BiologicalNADADP-ribosyl Cyclase 1AMP-Activated Protein KinasesCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channel BlockersCyclic ADP-RiboseGlucoseNADNAD(P)H Dehydrogenase (Quinone)NQO1 protein, humanOxygenRNA, Small Interfering

Identifiers

PMID25586669
PMCPMC4293602
OpenAlexW1967328591

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.