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BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma

The aim of the present study was to explore the role and biological function of bromodomain PHD finger transcription factor (BPTF) in T-cell lymphoma. Reverse transcription-quantitative PCR (RT-qPCR), western blotting, immunohistochemistry and bioinformatics analysis were used to determine the expre...

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Autores principales: Bai, Dongyu, Zhou, Yong, Shen, Fayan, Gao, Dehong, Suo, Wenhao, Zhang, Haiping, Li, Heng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9185150/
https://www.ncbi.nlm.nih.gov/pubmed/35720479
http://dx.doi.org/10.3892/ol.2022.13344
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author Bai, Dongyu
Zhou, Yong
Shen, Fayan
Gao, Dehong
Suo, Wenhao
Zhang, Haiping
Li, Heng
author_facet Bai, Dongyu
Zhou, Yong
Shen, Fayan
Gao, Dehong
Suo, Wenhao
Zhang, Haiping
Li, Heng
author_sort Bai, Dongyu
collection PubMed
description The aim of the present study was to explore the role and biological function of bromodomain PHD finger transcription factor (BPTF) in T-cell lymphoma. Reverse transcription-quantitative PCR (RT-qPCR), western blotting, immunohistochemistry and bioinformatics analysis were used to determine the expression levels of BPTF and Raf1 in T-cell lymphoma tissues and matched adjacent normal tissues. RT-qPCR and western blot analyses were used to examine the role of BPTF in the activation of MAPK signaling. The function of BPTF and Raf1 in T-cell lymphoma was investigated through in vitro and in vivo assays (MTT assay, colony formation assay, flow cytometry, western blotting, tumor xenograft model and TUNEL assay) following silencing and overexpression experiments in Hut-102 cells. The results demonstrated that BPTF and Raf1 were overexpressed in T-cell lymphoma tissues compared with normal tissues, and high expression of BPTF or Raf1 was associated with advanced clinical stage. BPTF promoted the activation of the MAPK pathway and was coexpressed with Raf1 in T-cell lymphoma tissues. Functional assays demonstrated that silencing of BPTF or Raf1 in Hut-102 cells suppressed cell proliferation and induced apoptosis. Furthermore, the carcinogenic effect of BPTF was confirmed by xenograft experiments in nude mice. The present findings suggested that BPTF may function as a crucial oncogenic factor and may serve as a novel therapeutic target in T-cell lymphoma.
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spelling pubmed-91851502022-06-16 BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma Bai, Dongyu Zhou, Yong Shen, Fayan Gao, Dehong Suo, Wenhao Zhang, Haiping Li, Heng Oncol Lett Articles The aim of the present study was to explore the role and biological function of bromodomain PHD finger transcription factor (BPTF) in T-cell lymphoma. Reverse transcription-quantitative PCR (RT-qPCR), western blotting, immunohistochemistry and bioinformatics analysis were used to determine the expression levels of BPTF and Raf1 in T-cell lymphoma tissues and matched adjacent normal tissues. RT-qPCR and western blot analyses were used to examine the role of BPTF in the activation of MAPK signaling. The function of BPTF and Raf1 in T-cell lymphoma was investigated through in vitro and in vivo assays (MTT assay, colony formation assay, flow cytometry, western blotting, tumor xenograft model and TUNEL assay) following silencing and overexpression experiments in Hut-102 cells. The results demonstrated that BPTF and Raf1 were overexpressed in T-cell lymphoma tissues compared with normal tissues, and high expression of BPTF or Raf1 was associated with advanced clinical stage. BPTF promoted the activation of the MAPK pathway and was coexpressed with Raf1 in T-cell lymphoma tissues. Functional assays demonstrated that silencing of BPTF or Raf1 in Hut-102 cells suppressed cell proliferation and induced apoptosis. Furthermore, the carcinogenic effect of BPTF was confirmed by xenograft experiments in nude mice. The present findings suggested that BPTF may function as a crucial oncogenic factor and may serve as a novel therapeutic target in T-cell lymphoma. D.A. Spandidos 2022-05-25 /pmc/articles/PMC9185150/ /pubmed/35720479 http://dx.doi.org/10.3892/ol.2022.13344 Text en Copyright: © Bai et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Bai, Dongyu
Zhou, Yong
Shen, Fayan
Gao, Dehong
Suo, Wenhao
Zhang, Haiping
Li, Heng
BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma
title BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma
title_full BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma
title_fullStr BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma
title_full_unstemmed BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma
title_short BPTF activates the MAPK pathway through coexpression with Raf1 to promote proliferation of T-cell lymphoma
title_sort bptf activates the mapk pathway through coexpression with raf1 to promote proliferation of t-cell lymphoma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9185150/
https://www.ncbi.nlm.nih.gov/pubmed/35720479
http://dx.doi.org/10.3892/ol.2022.13344
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