Evidence map›Paper›PMID 30284230›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2019

Hydrogen peroxide-induced mitophagy contributes to laryngeal cancer cells survival via the upregulation of FUNDC1.

L Hui, H Wu, T-W Wang, N Yang, X Guo, X-J Jang

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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

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  16. Mitochondrial-derived vesicles: Recent insights.Journal of cellular and molecular medicine · 2022
    Review
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  20. Induction and Detection of Mitophagy.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
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

6 authors at 1 institution in 1 country.

L HuiDepartment of Otolaryngology, The First Hospital of China Medical University, No. 155 Nanjing Bei Street, Shenyang, 110001, People's Republic of China. HuiLian_CMU@hotmail.com.ORCID http://orcid.org/0000-0002-1444-1056
H WuDepartment of Otolaryngology, The First Hospital of China Medical University, No. 155 Nanjing Bei Street, Shenyang, 110001, People's Republic of China.
T-W WangBishop Alemany High School, Mission Hills, CA, USA.
N YangDepartment of Otolaryngology, The First Hospital of China Medical University, No. 155 Nanjing Bei Street, Shenyang, 110001, People's Republic of China.
X GuoDepartment of Otolaryngology, The First Hospital of China Medical University, No. 155 Nanjing Bei Street, Shenyang, 110001, People's Republic of China.
X-J JangDepartment of Otolaryngology, The First Hospital of China Medical University, No. 155 Nanjing Bei Street, Shenyang, 110001, People's Republic of China.
First Hospital of China Medical University · CN

Funding

The Natural Science Foundation of Liaoning Province of P. R. China 201202287
6 · The paper itself

Abstract

purposeThe purpose of our study was to investigate an underlying mechanism that hydrogen peroxide-induced mitophagy contributed to laryngeal cancer cells survivals under oxidative stress condition.

methodsTumor tissue and serum samples were collected from patients with laryngeal cancer. The Hep2 cell, a human laryngeal carcinoma cell, was used in in vitro experiments. The levels of lipid peroxidation were analyzed by ELISA. Knockdown of FUNDC1 was performed by RNAi. The changes of target proteins were determined by qRT-PCR and western blot. The cells were analyzed for changes in proliferation using cell counting kit-8 and mitophagy by the mitochondrial membrane potential assay and transmission electron microscopy.

resultsFUNDC1 in laryngeal cancer tissues were relative to the levels of lipid peroxidation in laryngeal cancer patients, which suggested that FUNDC1 was associated with the status of oxidative stress in the laryngeal cancer patients. Hydrogen peroxide significantly induced the elevation of FUNDC1, a mitophagic factor, in a time- and dose-dependent manner in laryngeal cancer cells, which was dependent on ERK signal activation. Knockdown of FUNDC1 by the siRNA attenuated the survival of laryngeal cancer cells under hydrogen peroxide stimulation. Moreover, the elevated FUNDC1 was required for the occurrence of mitophagy under hydrogen peroxide stimulation, which was identified by transmission electron microscopy, the alterations of mitochondrial permeability transition and the specific mitochondrial protein, hsp60. Inhibition of mitophagy with cyclosporine A could also effectively attenuate the laryngeal cancer cells survival under hydrogen peroxide stimulation.

conclusionsHydrogen peroxide upregulated the expression of FUNDC1 through the activation of ERK1/2 signal to trigger a mitophagic response, giving laryngeal cancer cells a befit for survival. These findings suggested that FUNDC1 might be a potential target for the treatment of laryngeal cancer accompanied with high lipid peroxidation status.

Indexed as

Gene Expression Regulation, NeoplasticLipid PeroxidationMitophagyBiomarkers, TumorCase-Control StudiesCell SurvivalFollow-Up StudiesHumansHydrogen PeroxideLaryngeal NeoplasmsMembrane ProteinsMitochondriaMitochondrial ProteinsOxidantsPhosphorylationPrognosisBiomarkers, TumorFUNDC1 protein, humanHydrogen PeroxideMembrane ProteinsMitochondrial ProteinsOxidantsCell survivalFUNDC1Hydrogen peroxideLaryngeal cancerMitophagy

Identifiers

PMID30284230
OpenAlexW2895763175

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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.