GlutaredoxinV1, Main, Exploration, bibRecord, 000230

Proteomics-based investigation of multiple stages of OSCC development indicates that the inhibition of Trx-1 delays oral malignant transformation.

Identifieur interne : 000230 ( Main/Exploration ); précédent : 000229; suivant : 000231

Proteomics-based investigation of multiple stages of OSCC development indicates that the inhibition of Trx-1 delays oral malignant transformation.

Auteurs : Xijuan Chen [République populaire de Chine] ; Qinchao Hu [République populaire de Chine] ; Tong Wu [République populaire de Chine] ; Chunyang Wang [République populaire de Chine] ; Juan Xia [République populaire de Chine] ; Linglan Yang [République populaire de Chine] ; Bin Cheng [République populaire de Chine] ; Xiaobing Chen [République populaire de Chine]

Source :

International journal of oncology [ 1791-2423 ] ; 2018.

RBID : pubmed:29328386

Descripteurs français

KwdFr :
- 4-Nitro-quinoléine-1-oxyde (toxicité), Adulte (MeSH), Adulte d'âge moyen (MeSH), Animaux (MeSH), Apoptose (MeSH), Carcinogenèse (anatomopathologie), Carcinogenèse (effets des médicaments et des substances chimiques), Carcinome épidermoïde (anatomopathologie), Carcinome épidermoïde (chirurgie), Carcinome épidermoïde (induit chimiquement), Disulfures (pharmacologie), Espèces réactives de l'oxygène (métabolisme), Femelle (MeSH), Humains (MeSH), Imidazoles (pharmacologie), Langue (anatomopathologie), Lignée cellulaire tumorale (MeSH), Marqueurs biologiques tumoraux (métabolisme), Muqueuse de la bouche (anatomopathologie), Mâle (MeSH), Procédures de chirurgie orthognathique (MeSH), Protéomique (MeSH), Quinolinone (toxicité), Rat Sprague-Dawley (MeSH), Stress oxydatif (MeSH), Sujet âgé (MeSH), Thiorédoxines (antagonistes et inhibiteurs), Thiorédoxines (métabolisme), Transformation cellulaire néoplasique (anatomopathologie), Transformation cellulaire néoplasique (effets des médicaments et des substances chimiques), Tumeurs de la bouche (anatomopathologie), Tumeurs de la bouche (chirurgie), Tumeurs de la bouche (induit chimiquement), Tumeurs expérimentales (anatomopathologie), Tumeurs expérimentales (induit chimiquement), États précancéreux (anatomopathologie), États précancéreux (induit chimiquement).
MESH :
- anatomopathologie : Carcinogenèse, Carcinome épidermoïde, Langue, Muqueuse de la bouche, Transformation cellulaire néoplasique, Tumeurs de la bouche, Tumeurs expérimentales, États précancéreux.
- antagonistes et inhibiteurs : Thiorédoxines.
- chirurgie : Carcinome épidermoïde, Tumeurs de la bouche.
- effets des médicaments et des substances chimiques : Carcinogenèse, Transformation cellulaire néoplasique.
- induit chimiquement : Carcinome épidermoïde, Tumeurs de la bouche, Tumeurs expérimentales, États précancéreux.
- métabolisme : Espèces réactives de l'oxygène, Marqueurs biologiques tumoraux, Thiorédoxines.
- pharmacologie : Disulfures, Imidazoles.
- toxicité : 4-Nitro-quinoléine-1-oxyde, Quinolinone.
- Adulte, Adulte d'âge moyen, Animaux, Apoptose, Femelle, Humains, Lignée cellulaire tumorale, Mâle, Procédures de chirurgie orthognathique, Protéomique, Rat Sprague-Dawley, Stress oxydatif, Sujet âgé.

English descriptors

KwdEn :
- 4-Nitroquinoline-1-oxide (toxicity), Adult (MeSH), Aged (MeSH), Animals (MeSH), Apoptosis (MeSH), Biomarkers, Tumor (metabolism), Carcinogenesis (drug effects), Carcinogenesis (pathology), Carcinoma, Squamous Cell (chemically induced), Carcinoma, Squamous Cell (pathology), Carcinoma, Squamous Cell (surgery), Cell Line, Tumor (MeSH), Cell Transformation, Neoplastic (drug effects), Cell Transformation, Neoplastic (pathology), Disulfides (pharmacology), Female (MeSH), Humans (MeSH), Imidazoles (pharmacology), Male (MeSH), Middle Aged (MeSH), Mouth Mucosa (pathology), Mouth Neoplasms (chemically induced), Mouth Neoplasms (pathology), Mouth Neoplasms (surgery), Neoplasms, Experimental (chemically induced), Neoplasms, Experimental (pathology), Orthognathic Surgical Procedures (MeSH), Oxidative Stress (MeSH), Precancerous Conditions (chemically induced), Precancerous Conditions (pathology), Proteomics (MeSH), Quinolones (toxicity), Rats, Sprague-Dawley (MeSH), Reactive Oxygen Species (metabolism), Thioredoxins (antagonists & inhibitors), Thioredoxins (metabolism), Tongue (pathology).
MESH :
- chemical , antagonists & inhibitors : Thioredoxins.
- chemical , metabolism : Biomarkers, Tumor, Reactive Oxygen Species, Thioredoxins.
- chemical , pharmacology : Disulfides, Imidazoles.
- chemical , toxicity : 4-Nitroquinoline-1-oxide, Quinolones.
- chemically induced : Carcinoma, Squamous Cell, Mouth Neoplasms, Neoplasms, Experimental, Precancerous Conditions.
- drug effects : Carcinogenesis, Cell Transformation, Neoplastic.
- pathology : Carcinogenesis, Carcinoma, Squamous Cell, Cell Transformation, Neoplastic, Mouth Mucosa, Mouth Neoplasms, Neoplasms, Experimental, Precancerous Conditions, Tongue.
- surgery : Carcinoma, Squamous Cell, Mouth Neoplasms.
- Adult, Aged, Animals, Apoptosis, Cell Line, Tumor, Female, Humans, Male, Middle Aged, Orthognathic Surgical Procedures, Oxidative Stress, Proteomics, Rats, Sprague-Dawley.

Abstract

The majority of cases of oral squamous cell carcinoma (OSCC) develop from oral potentially malignant disorders, which have been confirmed to be involved in chronic oxidative stimulation. However, no effective treatment approaches have been used to prevent the development of dysplasia into cancerous lesions thus far. In the present study, a well-established OSCC model was used to detect proteomics profiles at different stages during oral malignant transformation. Of the 15 proteins that were found to be upregulated in both the dysplasia and carcinoma stages, the oxidative stress-associated proteins, thioredoxin-1 (Trx-1), glutaredoxin-1 and peroxiredoxin-2 were note as the proteins with significant changes in expression Trx-1 was identified to be the most significantly upregulated protein in the precancerous stage. Validation experiments confirmed that Trx-1 was overexpressed both in dysplasia and cancerous tissue samples, and the inhibition of Trx-1 was able to promote the apoptosis of OSCC cells under hypoxic conditions. Furthermore, the experimental application of a Trx-1-specific inhibitory agent in an animal model led to a lower cancerization rate and a delay in tumor formation. The possible mechanisms were associated with the increased apoptosis via a reactive oxygen species (ROS)-dependent pathway. Taken together, our findings indicate that Trx-1 may be an important target for delaying oral malignant transformation, which provides a novel therapeutic strategy for the prevention and treatment of OSCC.

DOI: 10.3892/ijo.2018.4235
PubMed: 29328386
PubMed Central: PMC5807042

Affiliations:

République populaire de Chine

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000272
to stream Main, to step Curation: 000272

Le document en format XML

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<author><name sortKey="Wang, Chunyang" sort="Wang, Chunyang" uniqKey="Wang C" first="Chunyang" last="Wang">Chunyang Wang</name>
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<author><name sortKey="Xia, Juan" sort="Xia, Juan" uniqKey="Xia J" first="Juan" last="Xia">Juan Xia</name>
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<author><name sortKey="Yang, Linglan" sort="Yang, Linglan" uniqKey="Yang L" first="Linglan" last="Yang">Linglan Yang</name>
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<author><name sortKey="Cheng, Bin" sort="Cheng, Bin" uniqKey="Cheng B" first="Bin" last="Cheng">Bin Cheng</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>4-Nitroquinoline-1-oxide (toxicity)</term>
<term>Adult (MeSH)</term>
<term>Aged (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Apoptosis (MeSH)</term>
<term>Biomarkers, Tumor (metabolism)</term>
<term>Carcinogenesis (drug effects)</term>
<term>Carcinogenesis (pathology)</term>
<term>Carcinoma, Squamous Cell (chemically induced)</term>
<term>Carcinoma, Squamous Cell (pathology)</term>
<term>Carcinoma, Squamous Cell (surgery)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Transformation, Neoplastic (drug effects)</term>
<term>Cell Transformation, Neoplastic (pathology)</term>
<term>Disulfides (pharmacology)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Imidazoles (pharmacology)</term>
<term>Male (MeSH)</term>
<term>Middle Aged (MeSH)</term>
<term>Mouth Mucosa (pathology)</term>
<term>Mouth Neoplasms (chemically induced)</term>
<term>Mouth Neoplasms (pathology)</term>
<term>Mouth Neoplasms (surgery)</term>
<term>Neoplasms, Experimental (chemically induced)</term>
<term>Neoplasms, Experimental (pathology)</term>
<term>Orthognathic Surgical Procedures (MeSH)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Precancerous Conditions (chemically induced)</term>
<term>Precancerous Conditions (pathology)</term>
<term>Proteomics (MeSH)</term>
<term>Quinolones (toxicity)</term>
<term>Rats, Sprague-Dawley (MeSH)</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>Thioredoxins (antagonists & inhibitors)</term>
<term>Thioredoxins (metabolism)</term>
<term>Tongue (pathology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>4-Nitro-quinoléine-1-oxyde (toxicité)</term>
<term>Adulte (MeSH)</term>
<term>Adulte d'âge moyen (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Apoptose (MeSH)</term>
<term>Carcinogenèse (anatomopathologie)</term>
<term>Carcinogenèse (effets des médicaments et des substances chimiques)</term>
<term>Carcinome épidermoïde (anatomopathologie)</term>
<term>Carcinome épidermoïde (chirurgie)</term>
<term>Carcinome épidermoïde (induit chimiquement)</term>
<term>Disulfures (pharmacologie)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Imidazoles (pharmacologie)</term>
<term>Langue (anatomopathologie)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Marqueurs biologiques tumoraux (métabolisme)</term>
<term>Muqueuse de la bouche (anatomopathologie)</term>
<term>Mâle (MeSH)</term>
<term>Procédures de chirurgie orthognathique (MeSH)</term>
<term>Protéomique (MeSH)</term>
<term>Quinolinone (toxicité)</term>
<term>Rat Sprague-Dawley (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
<term>Sujet âgé (MeSH)</term>
<term>Thiorédoxines (antagonistes et inhibiteurs)</term>
<term>Thiorédoxines (métabolisme)</term>
<term>Transformation cellulaire néoplasique (anatomopathologie)</term>
<term>Transformation cellulaire néoplasique (effets des médicaments et des substances chimiques)</term>
<term>Tumeurs de la bouche (anatomopathologie)</term>
<term>Tumeurs de la bouche (chirurgie)</term>
<term>Tumeurs de la bouche (induit chimiquement)</term>
<term>Tumeurs expérimentales (anatomopathologie)</term>
<term>Tumeurs expérimentales (induit chimiquement)</term>
<term>États précancéreux (anatomopathologie)</term>
<term>États précancéreux (induit chimiquement)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Thioredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers, Tumor</term>
<term>Reactive Oxygen Species</term>
<term>Thioredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Disulfides</term>
<term>Imidazoles</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>4-Nitroquinoline-1-oxide</term>
<term>Quinolones</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinogenèse</term>
<term>Carcinome épidermoïde</term>
<term>Langue</term>
<term>Muqueuse de la bouche</term>
<term>Transformation cellulaire néoplasique</term>
<term>Tumeurs de la bouche</term>
<term>Tumeurs expérimentales</term>
<term>États précancéreux</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Thiorédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Mouth Neoplasms</term>
<term>Neoplasms, Experimental</term>
<term>Precancerous Conditions</term>
</keywords>
<keywords scheme="MESH" qualifier="chirurgie" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Tumeurs de la bouche</term>
</keywords>
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<term>Cell Transformation, Neoplastic</term>
</keywords>
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<term>Tumeurs de la bouche</term>
<term>Tumeurs expérimentales</term>
<term>États précancéreux</term>
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<term>Marqueurs biologiques tumoraux</term>
<term>Thiorédoxines</term>
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<term>Carcinoma, Squamous Cell</term>
<term>Cell Transformation, Neoplastic</term>
<term>Mouth Mucosa</term>
<term>Mouth Neoplasms</term>
<term>Neoplasms, Experimental</term>
<term>Precancerous Conditions</term>
<term>Tongue</term>
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<term>Imidazoles</term>
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<keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
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<term>Quinolinone</term>
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<term>Aged</term>
<term>Animals</term>
<term>Apoptosis</term>
<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Orthognathic Surgical Procedures</term>
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<term>Proteomics</term>
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<term>Adulte d'âge moyen</term>
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<term>Femelle</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Mâle</term>
<term>Procédures de chirurgie orthognathique</term>
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<front><div type="abstract" xml:lang="en">The majority of cases of oral squamous cell carcinoma (OSCC) develop from oral potentially malignant disorders, which have been confirmed to be involved in chronic oxidative stimulation. However, no effective treatment approaches have been used to prevent the development of dysplasia into cancerous lesions thus far. In the present study, a well-established OSCC model was used to detect proteomics profiles at different stages during oral malignant transformation. Of the 15 proteins that were found to be upregulated in both the dysplasia and carcinoma stages, the oxidative stress-associated proteins, thioredoxin-1 (Trx-1), glutaredoxin-1 and peroxiredoxin-2 were note as the proteins with significant changes in expression Trx-1 was identified to be the most significantly upregulated protein in the precancerous stage. Validation experiments confirmed that Trx-1 was overexpressed both in dysplasia and cancerous tissue samples, and the inhibition of Trx-1 was able to promote the apoptosis of OSCC cells under hypoxic conditions. Furthermore, the experimental application of a Trx-1-specific inhibitory agent in an animal model led to a lower cancerization rate and a delay in tumor formation. The possible mechanisms were associated with the increased apoptosis via a reactive oxygen species (ROS)-dependent pathway. Taken together, our findings indicate that Trx-1 may be an important target for delaying oral malignant transformation, which provides a novel therapeutic strategy for the prevention and treatment of OSCC.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>08</Month>
<Day>31</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>12</Month>
<Day>28</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1791-2423</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>52</Volume>
<Issue>3</Issue>
<PubDate><Year>2018</Year>
<Month>Mar</Month>
</PubDate>
</JournalIssue>
<Title>International journal of oncology</Title>
<ISOAbbreviation>Int J Oncol</ISOAbbreviation>
</Journal>
<ArticleTitle>Proteomics-based investigation of multiple stages of OSCC development indicates that the inhibition of Trx-1 delays oral malignant transformation.</ArticleTitle>
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<Abstract><AbstractText>The majority of cases of oral squamous cell carcinoma (OSCC) develop from oral potentially malignant disorders, which have been confirmed to be involved in chronic oxidative stimulation. However, no effective treatment approaches have been used to prevent the development of dysplasia into cancerous lesions thus far. In the present study, a well-established OSCC model was used to detect proteomics profiles at different stages during oral malignant transformation. Of the 15 proteins that were found to be upregulated in both the dysplasia and carcinoma stages, the oxidative stress-associated proteins, thioredoxin-1 (Trx-1), glutaredoxin-1 and peroxiredoxin-2 were note as the proteins with significant changes in expression Trx-1 was identified to be the most significantly upregulated protein in the precancerous stage. Validation experiments confirmed that Trx-1 was overexpressed both in dysplasia and cancerous tissue samples, and the inhibition of Trx-1 was able to promote the apoptosis of OSCC cells under hypoxic conditions. Furthermore, the experimental application of a Trx-1-specific inhibitory agent in an animal model led to a lower cancerization rate and a delay in tumor formation. The possible mechanisms were associated with the increased apoptosis via a reactive oxygen species (ROS)-dependent pathway. Taken together, our findings indicate that Trx-1 may be an important target for delaying oral malignant transformation, which provides a novel therapeutic strategy for the prevention and treatment of OSCC.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Xijuan</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Qinchao</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Tong</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Chunyang</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
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<ForeName>Juan</ForeName>
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<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
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<ForeName>Linglan</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Bin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Xiaobing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510060, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
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<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>01</Month>
<Day>03</Day>
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<name sortKey="Wang, Chunyang" sort="Wang, Chunyang" uniqKey="Wang C" first="Chunyang" last="Wang">Chunyang Wang</name>
<name sortKey="Wu, Tong" sort="Wu, Tong" uniqKey="Wu T" first="Tong" last="Wu">Tong Wu</name>
<name sortKey="Xia, Juan" sort="Xia, Juan" uniqKey="Xia J" first="Juan" last="Xia">Juan Xia</name>
<name sortKey="Yang, Linglan" sort="Yang, Linglan" uniqKey="Yang L" first="Linglan" last="Yang">Linglan Yang</name>
</country>
</tree>
</affiliations>
</record>

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{{Explor lien
   |wiki=    Bois
   |area=    GlutaredoxinV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:29328386
   |texte=   Proteomics-based investigation of multiple stages of OSCC development indicates that the inhibition of Trx-1 delays oral malignant transformation.
}}

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       | NlmPubMed2Wicri -a GlutaredoxinV1

This area was generated with Dilib version V0.6.37.
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	Serveur d'exploration sur la glutarédoxine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la glutarédoxine

Proteomics-based investigation of multiple stages of OSCC development indicates that the inhibition of Trx-1 delays oral malignant transformation.

Proteomics-based investigation of multiple stages of OSCC development indicates that the inhibition of Trx-1 delays oral malignant transformation.

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