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DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway

To determine the differentially expressed proteins (DEPs) between paired samples of cervical cancer (CC) and paracancerous tissue by quantitative proteomics and to examine the effects of DUSP7 expression on the tumorigenesis and progression of CC. Proteomic profiles of three paired samples of CC and...

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Autores principales: Bai, Huimin, Song, Meiying, Jiao, Ruili, Li, Weihua, Zhao, Jing, Xiao, Meizhu, Jin, Mulan, Zhang, Zhengyu, Deng, Haiteng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8500958/
https://www.ncbi.nlm.nih.gov/pubmed/34435746
http://dx.doi.org/10.1111/jcmm.16865
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author Bai, Huimin
Song, Meiying
Jiao, Ruili
Li, Weihua
Zhao, Jing
Xiao, Meizhu
Jin, Mulan
Zhang, Zhengyu
Deng, Haiteng
author_facet Bai, Huimin
Song, Meiying
Jiao, Ruili
Li, Weihua
Zhao, Jing
Xiao, Meizhu
Jin, Mulan
Zhang, Zhengyu
Deng, Haiteng
author_sort Bai, Huimin
collection PubMed
description To determine the differentially expressed proteins (DEPs) between paired samples of cervical cancer (CC) and paracancerous tissue by quantitative proteomics and to examine the effects of DUSP7 expression on the tumorigenesis and progression of CC. Proteomic profiles of three paired samples of CC and paracancerous tissue were quantitatively analysed to identify DEPs. The relationship between DEP expression and patient clinicopathological characteristics and prognosis was evaluated. The effects of the selected DEPs on CC progression were examined in SIHA cells. A total of 129 DEPs were found. Western blot and immunohistochemistry (IHC) staining analyses confirmed the results from quantitative proteomic analysis showing that the selected DEP, HRAS, P‐ERK1/2, and PLD1 levels were increased, whereas the DUSP7 level was decreased in CC tissue compared with the paired normal paracancerous tissues. The IHC results from the CC TMA analysis showed that the decreased expression of DUSP7 (p = 0.045 and 0.044) was significantly associated with a tumour size >2 cm and parametrial infiltration. In addition, the decreased expression of DUSP7 and increased expression of p‐ERK1/2 were adversely related to patient relapse (p = 0.003 and 0.001) and survival (p = 0.034 and 0.006). The expression of HRAS and p‐ERK1/2 was decreased in DUSP7‐SIHA cells compared with NC‐SIHA cells (p = 0.0003 and 0.0026). Biological functions in vitro, including invasion, migration and proliferation and tumour formation in vivo were decreased in DUSP7‐SIHA cells (all p < 0.05) but increased in shDUSP7‐SIHA cells (all p < 0.05). DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway.
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spelling pubmed-85009582021-10-12 DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway Bai, Huimin Song, Meiying Jiao, Ruili Li, Weihua Zhao, Jing Xiao, Meizhu Jin, Mulan Zhang, Zhengyu Deng, Haiteng J Cell Mol Med Original Articles To determine the differentially expressed proteins (DEPs) between paired samples of cervical cancer (CC) and paracancerous tissue by quantitative proteomics and to examine the effects of DUSP7 expression on the tumorigenesis and progression of CC. Proteomic profiles of three paired samples of CC and paracancerous tissue were quantitatively analysed to identify DEPs. The relationship between DEP expression and patient clinicopathological characteristics and prognosis was evaluated. The effects of the selected DEPs on CC progression were examined in SIHA cells. A total of 129 DEPs were found. Western blot and immunohistochemistry (IHC) staining analyses confirmed the results from quantitative proteomic analysis showing that the selected DEP, HRAS, P‐ERK1/2, and PLD1 levels were increased, whereas the DUSP7 level was decreased in CC tissue compared with the paired normal paracancerous tissues. The IHC results from the CC TMA analysis showed that the decreased expression of DUSP7 (p = 0.045 and 0.044) was significantly associated with a tumour size >2 cm and parametrial infiltration. In addition, the decreased expression of DUSP7 and increased expression of p‐ERK1/2 were adversely related to patient relapse (p = 0.003 and 0.001) and survival (p = 0.034 and 0.006). The expression of HRAS and p‐ERK1/2 was decreased in DUSP7‐SIHA cells compared with NC‐SIHA cells (p = 0.0003 and 0.0026). Biological functions in vitro, including invasion, migration and proliferation and tumour formation in vivo were decreased in DUSP7‐SIHA cells (all p < 0.05) but increased in shDUSP7‐SIHA cells (all p < 0.05). DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway. John Wiley and Sons Inc. 2021-08-26 2021-10 /pmc/articles/PMC8500958/ /pubmed/34435746 http://dx.doi.org/10.1111/jcmm.16865 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Bai, Huimin
Song, Meiying
Jiao, Ruili
Li, Weihua
Zhao, Jing
Xiao, Meizhu
Jin, Mulan
Zhang, Zhengyu
Deng, Haiteng
DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway
title DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway
title_full DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway
title_fullStr DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway
title_full_unstemmed DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway
title_short DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway
title_sort dusp7 inhibits cervical cancer progression by inactivating the ras pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8500958/
https://www.ncbi.nlm.nih.gov/pubmed/34435746
http://dx.doi.org/10.1111/jcmm.16865
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