Cargando…

Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis

BACKGROUND: X-linked inhibitor of apoptosis (XIAP) is a vital factor in the anti-apoptosis mechanism of tumors and is highly expressed in renal cell carcinoma (RCC). However, the mechanism through which XIAP regulates DNA damage repair is unknown. This study investigated the regulatory mechanism of...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Tian-Shu, Chen, Chao, Zhou, Biao, Xia, Bo-Wen, Chen, Zong-Ping, Yan, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6964936/
https://www.ncbi.nlm.nih.gov/pubmed/31855962
http://dx.doi.org/10.1097/CM9.0000000000000553
_version_ 1783488554081452032
author Liu, Tian-Shu
Chen, Chao
Zhou, Biao
Xia, Bo-Wen
Chen, Zong-Ping
Yan, Yong
author_facet Liu, Tian-Shu
Chen, Chao
Zhou, Biao
Xia, Bo-Wen
Chen, Zong-Ping
Yan, Yong
author_sort Liu, Tian-Shu
collection PubMed
description BACKGROUND: X-linked inhibitor of apoptosis (XIAP) is a vital factor in the anti-apoptosis mechanism of tumors and is highly expressed in renal cell carcinoma (RCC). However, the mechanism through which XIAP regulates DNA damage repair is unknown. This study investigated the regulatory mechanism of XIAP in etoposide-induced apoptosis in two Caki-1 cell lines with high or low XIAP expression. METHODS: The two cell lines were established using RNA interference technology. The differentially expressed proteins in the two cell lines were globally analyzed through an isobaric tags for relative and absolute quantitation-based quantitative proteomics approach. Proteomic analysis revealed 255, 375, 362, and 5 differentially expressed proteins after 0, 0.5, 3, and 12 h of drug stimulation, respectively, between the two cell lines. The identified differentially expressed proteins were involved in numerous biological processes. In addition, the expression of histone proteins (H1.4, H2AX, H3.1, H3.2, and H3.3) was drastically altered, and the effects of XIAP silencing were accompanied by the marked downregulation of H2AX. Protein-protein interactions were assessed and confirmed through immunofluorescence and Western blot analyses. RESULTS: The results suggested that XIAP may act as a vital cell signal regulator that regulates the expression of DNA repair-related proteins, such as H2AX, and influences the DNA repair process. CONCLUSIONS: Given these functions, XIAP may be the decisive factor in determining the sensitivity of RCC cell apoptosis induction in response to chemotherapeutic agents.
format Online
Article
Text
id pubmed-6964936
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher Wolters Kluwer Health
record_format MEDLINE/PubMed
spelling pubmed-69649362020-02-10 Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis Liu, Tian-Shu Chen, Chao Zhou, Biao Xia, Bo-Wen Chen, Zong-Ping Yan, Yong Chin Med J (Engl) Original Articles BACKGROUND: X-linked inhibitor of apoptosis (XIAP) is a vital factor in the anti-apoptosis mechanism of tumors and is highly expressed in renal cell carcinoma (RCC). However, the mechanism through which XIAP regulates DNA damage repair is unknown. This study investigated the regulatory mechanism of XIAP in etoposide-induced apoptosis in two Caki-1 cell lines with high or low XIAP expression. METHODS: The two cell lines were established using RNA interference technology. The differentially expressed proteins in the two cell lines were globally analyzed through an isobaric tags for relative and absolute quantitation-based quantitative proteomics approach. Proteomic analysis revealed 255, 375, 362, and 5 differentially expressed proteins after 0, 0.5, 3, and 12 h of drug stimulation, respectively, between the two cell lines. The identified differentially expressed proteins were involved in numerous biological processes. In addition, the expression of histone proteins (H1.4, H2AX, H3.1, H3.2, and H3.3) was drastically altered, and the effects of XIAP silencing were accompanied by the marked downregulation of H2AX. Protein-protein interactions were assessed and confirmed through immunofluorescence and Western blot analyses. RESULTS: The results suggested that XIAP may act as a vital cell signal regulator that regulates the expression of DNA repair-related proteins, such as H2AX, and influences the DNA repair process. CONCLUSIONS: Given these functions, XIAP may be the decisive factor in determining the sensitivity of RCC cell apoptosis induction in response to chemotherapeutic agents. Wolters Kluwer Health 2019-12-20 2019-12-20 /pmc/articles/PMC6964936/ /pubmed/31855962 http://dx.doi.org/10.1097/CM9.0000000000000553 Text en Copyright © 2019 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license. http://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0
spellingShingle Original Articles
Liu, Tian-Shu
Chen, Chao
Zhou, Biao
Xia, Bo-Wen
Chen, Zong-Ping
Yan, Yong
Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis
title Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis
title_full Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis
title_fullStr Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis
title_full_unstemmed Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis
title_short Isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of X-linked inhibitor of apoptosis and H2AX in etoposide-induced renal cell carcinoma apoptosis
title_sort isobaric tags for relative and absolute quantitation-based quantitative proteomic analysis of x-linked inhibitor of apoptosis and h2ax in etoposide-induced renal cell carcinoma apoptosis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6964936/
https://www.ncbi.nlm.nih.gov/pubmed/31855962
http://dx.doi.org/10.1097/CM9.0000000000000553
work_keys_str_mv AT liutianshu isobarictagsforrelativeandabsolutequantitationbasedquantitativeproteomicanalysisofxlinkedinhibitorofapoptosisandh2axinetoposideinducedrenalcellcarcinomaapoptosis
AT chenchao isobarictagsforrelativeandabsolutequantitationbasedquantitativeproteomicanalysisofxlinkedinhibitorofapoptosisandh2axinetoposideinducedrenalcellcarcinomaapoptosis
AT zhoubiao isobarictagsforrelativeandabsolutequantitationbasedquantitativeproteomicanalysisofxlinkedinhibitorofapoptosisandh2axinetoposideinducedrenalcellcarcinomaapoptosis
AT xiabowen isobarictagsforrelativeandabsolutequantitationbasedquantitativeproteomicanalysisofxlinkedinhibitorofapoptosisandh2axinetoposideinducedrenalcellcarcinomaapoptosis
AT chenzongping isobarictagsforrelativeandabsolutequantitationbasedquantitativeproteomicanalysisofxlinkedinhibitorofapoptosisandh2axinetoposideinducedrenalcellcarcinomaapoptosis
AT yanyong isobarictagsforrelativeandabsolutequantitationbasedquantitativeproteomicanalysisofxlinkedinhibitorofapoptosisandh2axinetoposideinducedrenalcellcarcinomaapoptosis