Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma

The key factors leading to transformed follicular lymphoma (t-FL) include the aberrations of epigenetic modifiers as early and driving events, especially mutations in the gene encoding for histone acetyltransferase. Therefore, reversal of this phenomenon by histone deacetylase (HDAC) inhibitors is e...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Mengya Zhong, Jinshui Tan, Guangchao Pan, Yuelong Jiang, Hui Zhou, Qian Lai, Qinwei Chen, Liyuan Fan, Manman Deng, Bing Xu, Jie Zha
Formato: article
Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://doaj.org/article/3d713885de444a33b83a276132d8180e
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:3d713885de444a33b83a276132d8180e
record_format dspace
spelling oai:doaj.org-article:3d713885de444a33b83a276132d8180e2021-12-03T05:09:55ZPreclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma2234-943X10.3389/fonc.2021.780118https://doaj.org/article/3d713885de444a33b83a276132d8180e2021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fonc.2021.780118/fullhttps://doaj.org/toc/2234-943XThe key factors leading to transformed follicular lymphoma (t-FL) include the aberrations of epigenetic modifiers as early and driving events, especially mutations in the gene encoding for histone acetyltransferase. Therefore, reversal of this phenomenon by histone deacetylase (HDAC) inhibitors is essential for the development of new treatment strategies in t-FL. Several t-FL cell lines were treated with various doses of chidamide and subjected to cell proliferation, apoptosis and cell cycle analyses with CCK-8 assay, Annexin V/PI assay and flow cytometry, respectively. Chidamide dose-dependently inhibited cell proliferation, caused G0/G1 cycle arrest and triggered apoptosis in t-FL cells. In addition, the effects of chidamide on tumor growth were evaluated in vivo in xenograft models. RNA-seq analysis revealed gene expression alterations involving the PI3K-AKT signaling pathway might account for the mechanism underlying the antitumor activity of chidamide as a single agent in t-FL. These findings provide a basis for further clinical exploration of chidamide as a promising treatment for FL.Mengya ZhongMengya ZhongJinshui TanJinshui TanGuangchao PanGuangchao PanYuelong JiangYuelong JiangHui ZhouHui ZhouQian LaiQian LaiQinwei ChenQinwei ChenLiyuan FanLiyuan FanManman DengManman DengBing XuBing XuJie ZhaJie ZhaFrontiers Media S.A.articletransformed-follicular lymphoma (t-FL)chidamideHDACPI3K/AKT signalingepigenetic antitumor therapyNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENFrontiers in Oncology, Vol 11 (2021)
institution DOAJ
collection DOAJ
language EN
topic transformed-follicular lymphoma (t-FL)
chidamide
HDAC
PI3K/AKT signaling
epigenetic antitumor therapy
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
spellingShingle transformed-follicular lymphoma (t-FL)
chidamide
HDAC
PI3K/AKT signaling
epigenetic antitumor therapy
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Mengya Zhong
Mengya Zhong
Jinshui Tan
Jinshui Tan
Guangchao Pan
Guangchao Pan
Yuelong Jiang
Yuelong Jiang
Hui Zhou
Hui Zhou
Qian Lai
Qian Lai
Qinwei Chen
Qinwei Chen
Liyuan Fan
Liyuan Fan
Manman Deng
Manman Deng
Bing Xu
Bing Xu
Jie Zha
Jie Zha
Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma
description The key factors leading to transformed follicular lymphoma (t-FL) include the aberrations of epigenetic modifiers as early and driving events, especially mutations in the gene encoding for histone acetyltransferase. Therefore, reversal of this phenomenon by histone deacetylase (HDAC) inhibitors is essential for the development of new treatment strategies in t-FL. Several t-FL cell lines were treated with various doses of chidamide and subjected to cell proliferation, apoptosis and cell cycle analyses with CCK-8 assay, Annexin V/PI assay and flow cytometry, respectively. Chidamide dose-dependently inhibited cell proliferation, caused G0/G1 cycle arrest and triggered apoptosis in t-FL cells. In addition, the effects of chidamide on tumor growth were evaluated in vivo in xenograft models. RNA-seq analysis revealed gene expression alterations involving the PI3K-AKT signaling pathway might account for the mechanism underlying the antitumor activity of chidamide as a single agent in t-FL. These findings provide a basis for further clinical exploration of chidamide as a promising treatment for FL.
format article
author Mengya Zhong
Mengya Zhong
Jinshui Tan
Jinshui Tan
Guangchao Pan
Guangchao Pan
Yuelong Jiang
Yuelong Jiang
Hui Zhou
Hui Zhou
Qian Lai
Qian Lai
Qinwei Chen
Qinwei Chen
Liyuan Fan
Liyuan Fan
Manman Deng
Manman Deng
Bing Xu
Bing Xu
Jie Zha
Jie Zha
author_facet Mengya Zhong
Mengya Zhong
Jinshui Tan
Jinshui Tan
Guangchao Pan
Guangchao Pan
Yuelong Jiang
Yuelong Jiang
Hui Zhou
Hui Zhou
Qian Lai
Qian Lai
Qinwei Chen
Qinwei Chen
Liyuan Fan
Liyuan Fan
Manman Deng
Manman Deng
Bing Xu
Bing Xu
Jie Zha
Jie Zha
author_sort Mengya Zhong
title Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma
title_short Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma
title_full Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma
title_fullStr Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma
title_full_unstemmed Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma
title_sort preclinical evaluation of the hdac inhibitor chidamide in transformed follicular lymphoma
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/3d713885de444a33b83a276132d8180e
work_keys_str_mv AT mengyazhong preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT mengyazhong preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT jinshuitan preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT jinshuitan preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT guangchaopan preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT guangchaopan preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT yuelongjiang preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT yuelongjiang preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT huizhou preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT huizhou preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT qianlai preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT qianlai preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT qinweichen preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT qinweichen preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT liyuanfan preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT liyuanfan preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT manmandeng preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT manmandeng preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT bingxu preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT bingxu preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT jiezha preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
AT jiezha preclinicalevaluationofthehdacinhibitorchidamideintransformedfollicularlymphoma
_version_ 1718373925268750336