Evidence map›Paper›PMID 31940844›Full record

ArticleInternational journal of molecular sciences2020

Impaired Glycolysis Promotes AlcoholExposure-Induced Apoptosis in HEI-OC1 Cells via Inhibition of EGFR Signaling.

Hyunsook Kang, Seong Jun Choi, Kye Hoon Park, Chi-Kyou Lee, Jong-Seok Moon

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 45% 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

9 citing papers in PubMed, 12 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

5 authors at 1 institution in 1 country.

Hyunsook KangDepartment of Otorhinoaryngology-Head and Neck Surgery, College of Medicine, Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea.
Seong Jun ChoiDepartment of Otorhinoaryngology-Head and Neck Surgery, College of Medicine, Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea.
Kye Hoon ParkDepartment of Otorhinoaryngology-Head and Neck Surgery, College of Medicine, Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea.
Chi-Kyou LeeDepartment of Otorhinoaryngology-Head and Neck Surgery, College of Medicine, Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea.ORCID 0000-0001-5380-1651
Jong-Seok MoonDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si, Chungcheongnam-do 31151, Korea.
Soonchunhyang University · KR

Funding

National Research Foundation of Korea NRF-2019M3E5D1A02069071Soonchunhyang University Research Fund 2020
6 · The paper itself

Abstract

Glucose metabolism is an important metabolic pathway in the auditory system. Chronic alcohol exposure can cause metabolic dysfunction in auditory cells during hearing loss. While alcohol exposure has been linked to hearing loss, the mechanism by which impaired glycolysis promotes cytotoxicity and cell death in auditory cells remains unclear. Here, we show that the inhibition of epidermal growth factor receptor (EGFR)-induced glycolysis is a critical mechanism for alcohol exposure-induced apoptosis in HEI-OC1 cells. The cytotoxicity via apoptosis was significantly increased by alcohol exposure in HEI-OC1 cells. The glycolytic activity and the levels of hexokinase 1 (HK1) were significantly suppressed by alcohol exposure in HEI-OC1 cells. Mechanistic studies showed that the levels of EGFR and AKT phosphorylation were reduced by alcohol exposure in HEI-OC1 cells. Notably, HK1 expression and glycolytic activity was suppressed by EGFR inhibition in HEI-OC1 cells. These results suggest that impaired glycolysis promotes alcohol exposure-induced apoptosis in HEI-OC1 cells via the inhibition of EGFR signaling.

Indexed as

ApoptosisGlycolysisAnimalsCell LineErbB ReceptorsEthanolHair Cells, AuditoryHexokinaseMiceProto-Oncogene Proteins c-aktSignal TransductionErbB ReceptorsEthanolHexokinaseProto-Oncogene Proteins c-aktalcoholapoptosisEGFR signalingglycolysisHEI-OC1 cells

Identifiers

PMID31940844
PMCPMC7014033
OpenAlexW3000642788

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.