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trichostatin a improves the inflammatory response and liver injury in septic mice through the FoxO3a/autophagy signaling pathway

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World Journal of Emergency Medicine 2022年第3期13卷 182-188页

作者： Mei-jia Shen Li-chao Sun Xiao-yu Liu Meng-chen Xiong Shan Li A-ling Tang Guo-qiang Zhang Graduate School of Peking Union Medical College Chinese Academy of Medical Sciences/Peking Union Medical CollegeBeijing 100193China Emergency Department China-Japan Friendship HospitalBeijing 100029China Graduate School Beijing University of Chinese MedicineBeijing 100029China

BACKGROUND:Sepsis-induced liver injury is a fatal complication of *** A(TSA)regulates inflammation and autophagy in some human diseases,and forkhead box O3a(FoxO3a)has been shown to regulate *** present study aims to investigate whether TSA exerts its effects on septic liver injury through the FoxO3a/autophagy signaling ***:A sepsis mouse model was constructed by the cecal ligation and puncture(CLP)method,and AML12 cells were pretreated with lipopolysaccharide(LPS)(1μg/mL)to establish a sepsis cell *** mice were divided into four groups,namely control group,TSA group,CLP group,and CLP+TSA group,with 10 mice in each *** were divided into control group,TSA group,LPS group,and LPS+TSA ***-eosin(H&E)staining and biochemical methods were used to evaluate liver tissue ***-linked immunosorbent assay(ELISA)was applied to detect the expression of proinflammatory cytokines,and Western blotting and immunofluorescence were used to measure autophagy-related protein ***:Compared with the CLP group(mice),the proinflammatory cytokines(interleukin-β[IL-β]2,665.27±324.90 pg/mL to 2,080.26±373.66 pg/mL;interleukin-6[IL-6]399.01±60.98 pg/mL to 221.90±46.89 pg/mL)and the hepatocyte injury markers(aspartate transaminase[AST]from 198.18±27.07 U/L to 128.42±20.55 U/L;alanine aminotransferase[ALT]from 634.98±74.10 U/L to 478.60±32.56 U/L)were notably decreased after TSA ***,LC3 II and FoxO3a showed an obvious increase and P62 showed an obvious decrease in the CLP+TSA *** experiment results showed the similar *** Fox O3a gene was knocked down in AML12 cells,the promotion of autophagy and the improvement of liver enzyme index and inflammation by TSA were ***:TSA may improve the inflammatory response and liver injury in septic mice through Fox O3a/autophagy.

关键词： Sepsis Liver injury trichostatin a Autophagy Inflammation

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Function of c-Fos-like and c-Jun-like Proteins on trichostatin a-induced G2/M Arrest in Physarum polycephalum

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Acta Biochimica et Biophysica Sinica 2005年第11期37卷 767-772页

作者： Xiao-Xue LI Jun LU Yan-Mei ZHAO Bai-Qu HUANG Institute of Genetics and Cytology,Northeast Normal University,Changchun 130024,China Institute of Genetics and Cytology Northeast Normal UniversityChangchun 130024 China

The homologs of transcription factors c-Fos and c-Jun have been detected in slime moldPhysarum polycephalum during progression of the synchronous cell *** we demonstrated that c-Fos-like and c-Jun-like proteins participated in G2/M transition by the regulation of the level of Cyclin B1protein in *** study of antibody neutralization revealed that interruption of the functions ofc-Fos-like and c-Jun-like proteins resulted in G2/M transition arrest,implicating their functional roles in cellcycle *** G2/M transition was blocked by histone deacetylase inhibitor trichostatin a,changes inc-Fos- and c-Jun-like protein levels,and hyperacetylation of c-Jun-like protein,were *** datasuggest that in ***,c-Fos- and c-Jun-like proteins may be the key factors in the regulation ofhistone acetylation-related G2/M transition,involving the coordinated expression and hyperacetylation ofthese proteins.

关键词： c-Fos-like protein c-Jun-like protein trichostatin a G2/M transition Physarum polycephalum

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trichostatin a INHIBITS PROLIFERATION,INDUCES APOPTOSIS AND CELL CYCLE ARREST IN HELA CELLS

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Chinese Journal of Cancer Research 2006年第3期18卷 188-192页

作者：徐周敏汪宜群梅琪陈坚杜佳魏燕徐迎春 Department of Oncology Shanghai Corps Hospital Chinese People’s Armed Police Forces Shanghai 201103

Objective： The histone deacetylase inhibitors （HDACIS） have been shown to inhibit cancer cell proliferation, stimulate apoptosis, an induce cell cycle arrest. Our purpose was to investigate the antiproliferative effects of a HDACI, trichostatin a （TSA）, against human cervical cancer cells （HeLa）. Methods： HeLa cells were treated in vitro with various concentrations of TSA. The inhibitory effect of TSA on the growth of HeLa cells was measured by MTT assay. To detect the characteristic of apoptosis chromatin condensation, HeLa cells were stained with Hoechst 33258 in the presence of TSA. Induction of cell cycle arrest was studied by flow cytometry. Changes in gene expression of p53, p21wafl and p27Kipl were studied by semiquantitative RT-PCR. Results： TSA inhibited cell growth in a time- and dose-dependent manner. Hoechst 33258 staining assay showed that TSA induced apoptosis. Cell cycle analysis indicated that treatment with TSA decreased the proportion of cells in S phase and increased the proportion of cells in G0/G1 and/or G2/M phases of the cell cycle. This was concomitant with overexpression of genes related to malignant phenotype, including an increase in p53, p21wall and p27Kipl. Conclusion： These results suggest that TSA is effective in inhibiting growth of HeLa cells in vitro. The findings raise the possibility that TSA may prove particularly effective in treatment of cervical cancers.

关键词： trichostatin a HeLa cells Apoptosis Cell cycle Gene expression

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Cell-Cycle-Dependent Variations in the FTIR Spectroscopy of HeLa Cells Treated with trichostatin a

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光谱学与光谱分析 2011年第8期31卷 2076-2080页

作者： ZHANG Feng-qiu QI Jian YANG Zhan-guo School of Physical Engineering Zhengzhou University Zhengzhou 450052 China

It is quite complex to evaluate the mechanism of action for antitumor drugs on cancer *** have pointed out that there is an unique advantage of Fourier transform infrared spectrum to obtain a fingerprint of all molecules present in the cells when cancer cells were exposed to anti-cancer *** A(TSA) is a most potent reversible inhibitor of mammalian histone *** can inhibit cancer cell growth in vitro and in *** the present study,HeLa cells were exposed to 0,50,100,200,300 and 400 nmol·L-1 TSA,and FTIR spectra were applied to evaluate the effect of TSA on cancer *** show that there is some significant relationship between the changes in FTIR absorption and cell cycle *** the other hand,this investigation shows that the concentration of TSA had to be more than 200 nmol·L-1 in order to ensure A1 080 cm-1/A1 540 cm-1≥1 for inhibiting cell proliferation.

关键词： Fourier transform infrared spectrum trichostatin a Cell cycle

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Effect of trichostatin a and paclitaxel on the proliferation and apoptosis of lung adenocarcinoma cells

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Chinese Medical Journal 2013年第1期126卷 129-134页

作者： ZHANG Song ZHANG Qun-cheng JIANG Shu-juan Department of Respiratory Diseases Provincial Hospital Affiliatedto Shandong University Jinan Shandong 250021 China

Background Histone deacetylase inhibitors can regulate gene expression through modulation of the degree of acetylation of histone and non-histone, thus affecting cell proliferation, survival and chemosensitivity. Histone deacetylase inhibitors combined with paclitaxel may enhance the inhibitory effect of drugs on lung cancer cells. This study aimed to observe the effect of trichostatin a （TSA）/paclitaxel on the proliferation and apoptosis in human A549 lung adenocarcinoma cells, and to investigate its mechanism. Methods A549 cells were cultured in Dulbecco modified Eagle＇s medium （DMEM） in the presence of paclitaxel and the histone deacetylase inhibitor TSA, and the growth curve was obtained by trypan-blue exclusion assay and cell count. Apoptosis was assessed using Hoechst 33258 staining and flow cytometry analysis, and cell cycle was detected by flow cytometry analysis. The proteins poly ADP-ribose polymerase （PARP）, caspase-3, survivin, and tubulin acetylation were detected by Western blotting. Results A significant reduction of proliferation was observed in A549 lung adenocarcinoma cells treated by paclitaxel or TSA. Combined treatment with TSA/paclitaxel caused the greatest inhibition of cell proliferation. The combined treatment with TSA and paclitaxel induced more severe apoptosis, and significantly more cells were arrested in G2/M phase （P 〈0.05） then with a single drug. Using Western blotting, we demonstrated that treatment with TSNpaclitaxel led to synergistic increase in acetylated tubulin, PARP, caspase-3, and reduced the expression of survivin. Conclusion TSA and paclitaxel have a synergistic activity that can inhibit cell growth and induce apoptosis.

关键词： trichostatin a paclitaxel caspase-3 survivin

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Inhibitory Effects of 5-Aza-2'-Deoxycytidine and trichostatin a in Combination with p53-Expressing Adenovirus on Human Laryngocarcinoma Cells

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Chinese Journal of Cancer Research 2012年第3期24卷 232-237页

作者： Ling-yan Jiang Meng Lian Hong Wang Ju-gao Fang Qi Wang Key Laboratory of Otorhinolaryngology Head and Neck Surgery(Ministry of Education) Beijing Institute of OtorhinolaryngologyBeijing 100005China Department of Otorhmolaryngology Head and Neck Surgery Beijing Tongren HospitalCapital Medical UniversityBeijing 100730China

Objective： To investigate the effects of 5-Aza-2＇-deoxycytidine （5-Aza-Cdr） and trichostatin a （TSA） combined with p53-expressing adenovirus （Ad-p53） on Hep-2 cell line in vivo and in vitro, in order to explore its possibility in biological treatment of laryngocarcinoma. Methods： Effects of 5-Aza-Cdr and TSA in combination with Ad-p53 on Hep-2 cell line in vivo were determined by Cell Counting Kit-8 （CCK-8） assay. The effect of drug combination was calculated by Jin＇s formula. Effects on the cell line in vitro were investigated by establishing the nude mice model. Results： 5-Aza-Cdr and TSA showed inhibitory effects on the proliferation of Hep-2 cells in dose- and time-dependent manner. Ad-p53 can inhibit the growth of Hep-2 cells in vivo and in vitro. However, the combination of epigenetic reagents （5-Aza-Cdr/TSA） and Ad-p53 was less effective than individual use of Ad-p53. 5-Aza-Cdr and Ad-p53 inhibited the growth of transplanted tumors and reduced the volume of tumors, and the tumor volume of Ad-p53 group was significantly smaller than that of the control group （P0.05）. Conclusion： Both epigenetic reagents （5-Aza-Cdr/TSA） and Ad-p53 can suppress cell proliferation on Hep-2 in vivo and in vitro and there may be some antagonistic mechanism between Ad-p53 and epigenetic reagents （5-Aza-Cdr/ TSA）.

关键词： 5-Aza-'-deoxycytidine trichostatin a p-expressing adenovirus Hep-2cell line

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Gastric cancer cell lines induced by trichostatin a

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World Journal of Gastroenterology 2008年第30期14卷 4810-4815页

作者： Xiao-Ming Zou Yun-Long Li Hao Wang Wu Cui Xiao-Lin Li Song-Bin Fu Hong-Chi Jiang Department of General Surgery the Second Clinical College Harbin Medical University Harbin 150086 Heilongjiang Province China Laboratory of Medical Genetics Harbin Medical University Harbin 150081 Heilongjiang Province China Department of General Surgery the First Clinical College Harbin Medical University Harbin 150081 Heilongjiang Province China

AIM： To explore the effect of trichostatin a （TSA） on apoptosis and acetylated histone H3 levels in gastric cancer cell lines BGC-823 and SGC-7901. METHODS： The effect of TSA on growth inhibition and apoptosis was examined by MTT, fluorescence microscopy and PI single-labeled flow cytometry. The acetylated histone H3 level was detected by Western blot. RESULTS： TSA induced apoptosis in gastric cancer cell lines BGC-823 and SGC-7901 was in a dose and time-dependent manner. Apoptotic cells varied significantly between TSA treated groups （37.5 ng/mL 72 h for BGC-823 cell line and 75 ng/mL 72 h for SGC-7901 cell line） and control group （0.85 ± 0.14 vs 1.14 ± 0.07, P = 0.02; 0.94 ± 0.07 vs 1.15 ± 0.06, P = 0.02）. Morphologic changes of apoptosis, including nuclear chromatin condensation and fluorescence strength, were observed under fluorescence microscopy. TSA treatment in BGC-823 and SGC-7901 cell lines obviously induced cell apoptosis, which was demonstrated by the increased percentage of sub-G1 phase cells, the reduction of Gl-phase cells and the increase of apoptosis rates in flow cytometric analysis. The result of Western blot showed that the expression of acetylated histone H3 increased in BGC-823 and SGC-7901 TSA treatment groups as compared with the control ***： TSA can induce cell apoptosis in BGC-823 and SGC-7901 cell lines. The expression of acetylated histone H3 might be correlated with apoptosis.

关键词： BGC-823 SGC-7901 trichostatin a Apoptosis Acetylated histone H3 Gastric cancer

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Comparative Evaluation of the Effects of 5-Aza-2'-deoxycytidine and trichostatin a on Reactivation of hMLH1 in COC1/DDP Ovarian Cancer Cell Line

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Chinese Journal of Cancer Research 2009年第2期21卷 102-108页

作者： Chun-feng Meng Dong-qiu Dai Ke-jun Guo Department of Surgical Oncology Department of General Surgery Department of Gynecology First Affiliated Hospital China Medical University Shenyang 110001 China

Objective： hMLH1 protein serves to detect the DNA damage caused by cisplatin （DDP） and destroys the cell. The absence of hMLH1 expression has been correlated with acquired resistance of ovarian cancer cells to platinum. The aim of this study was to determine the possible role of DNA methylation and histone H3 lysine 9 （H3-K9） acetylation on the loss of hMLH1 expression, and to evaluate the reversal effects of 5-Aza-2＇-deoxycytidine （5-Aza-dC） and trichostatin a （TSA） on DDP-resistance in ovarian cancer cell lines. Methods： Two human ovarian cancer cell lines, COC1 and its DDP-resistant subline, COCI/DDP were cultured. The two cancer cells were treated with 5-Aza-dC or TSA. Using COC1 cells as a control, we used methylation-specific PCR （MSP） to analyze DNA methylation at hMLHI gene promoter, hMLH1 mRNA and protein expressions were analyzed by reverse transcriptase-polymerase chain reaction （RT-PCR） and Western blot. Chromatin immunoprecipitation assay （CHIP） was used to test the levels of histone H3-K9 acetylation at hMLH1 gene promoter. Results： In COC1 cells, there was no DNA methylation at hMLH1 gene promoter, while there were hMLH1 mRNA and protein expression. In COC1/DDP cells, there was DNA hypermethylation at hMLH1 gene promoter, while there was no hMLH1 mRNA or protein expression. The treatment with 5-Aza-dC resulted in DNA demethylation at the promoter region, as well as restoration of hMLH1 expression in COC1/DDP cells. The treatment with TSA had no effects on DNA demethylation or restoration of hMLH1 expression in COC1/DDP cells. Conclusion： Hypermethylation of DNA at the promoter is related to the silencing of hMLH1 in COC1/DDP ovarian cancer cells. DNA methylation at hMLH1 promoter could play a significant role in determining the sensitivity of ovarian cancer to DDP. The drug resistance mediated by methylation of hMLH1 could be overcome by 5-Aza-dC.

关键词： Ovarian cancer DNA methylation Drug resistance hMLH1 5-Aza-2'-deoxycytidine trichostatin a

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trichostatin a Regulates hGCN5 Expression and Cell Cycle on Daudi Cells in vitro

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第5期26卷 534-537页

作者：刘红利陈燕崔国惠伍钢王涛胡健莉 Cancer Center Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Department of Hematology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China

The expression of human general control of amino acid synthesis protein 5 （hGCN5） in human Burkitt＇s lymphoma Daudi cells in vitro, effects of trichostatin a （TSA） on cell proliferation and apoptosis and the molecular mechanism of TSA inhibiting proliferation of Daudi cells were investigated. The effects of TSA on the growth of Daudi cells were studied by 3-（4, 5-dimethyl-2-thiazolyl）-2,5-diphenyl-2H-tetrazolium （MTT） assay. The effect of TSA on the cell cycle of Daudi cells was assayed by a propidium iodide method. Immunochemistry and Western blot were used to detect the expression of hGCN5. The proliferation of Daudi cells was decreased in TSA-treated group with a 24 h IC50 value of 415.3979 μg/L. TSA induced apoptosis of Daudi cells in a timeand dose-dependent manner. Treatment with TSA （200 and 400 μg/L） for 24 h, the apoptosis rates of Daudi cells were （14.74±2.04） % and （17.63±1.25） %, respectively. The cell cycle was arrested in G0/G1 phase （50, 100 μg/L） and in G2/M phase （200 μg/L） by treatment with TSA for 24 h. The expression of hGCN5 protein in Daudi cells was increased in 24 h TSA-treated group by immunochemistry and Western blot （P〈0.05）. It was suggested that TSA as HDACIs could increase the expression of hGCN5 in Daudi cells, and might play an important role in regulating the proliferation and apoptosis of B-NHL cell line Daudi cells.

关键词： trichostatin a hGCN5 Burkitt's lymphoma Daudi

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Histone deacetylase inhibitor trichostatin a induced caspase-independent apoptosis in human gastric cancer cell

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Chinese Medical Journal 2007年第23期120卷 2112-2118页

作者： WU Zhi-qun ZHANG Rui Connie Chao ZHANG Ji-feng ZHANG Yuan-qiang Center of Cancer Therapy Tangdu Hospital The Fourth Military Medical University Xi＇an 710038 China Department of Histology and Embryology The Fourth Military Medical University Xi＇an 710032 China Section of Molecular Biology Division of Biological SciencesUniversity of California San Diego La Jolla California92093-0322 USA

Background Histone deacetylase inhibitors （HDACIs） have been reported to induce apoptosis in cancer cells. The effects of trichostatin a （TSA） on gastric cancer cells have not been well characterized. This study was aimed to explore the effects and mechanisms of TSA on human gastric cancer SGC-7901 cells. Methods The cells were treated with TSA and analyzed by cell proliferation assay, Western blot, TUNEL assay, flow cytometry by fluorescein isothiocyanate （FITC） conjugated with Annexin V and PI staining, immunofluorescence analysis, analysis of subcellular fractionation, gene chips and real time polymerase chain reaction （PCR）. Results TSA could inhibit cell growth and induced apoptosis in gastric cancer SGC-7901 cells through the regulation of apoptosis-related genes, such as Bcl-2, Bax and survivin. Further study indicated that the pan-caspase inhibitor z-VAD-fmk did not inhibit the apoptosis induced by TSA, and we did not observe the cleavage of poly ADP ribose polymerase （PARP） after TSA treatment too. In addition, apoptosis inducing factor （AIF） and EndoG were found to translocate from mitochondria to nucleus in the immunofluorescence assay and the Western analysis of subcellular fractionation confirmed the result of immunofluorescence assay. Conclusions The apoptosis induced by TSA in gastric cancer SGC-7901 cells involves a caspase-independent pathway.

关键词： gastric cancer histone deacetylase inhibitor trichostatin a apoptosis

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