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histone deacetylase inhibitor promotes differentiation of embryonic stem cells into neural cells in adherent monoculture

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Chinese Medical Journal 2010年第6期123卷 734-738页

作者： YAO Xing ZHANG Jia-rong HUANG Hua-rong DAI Li-cheng LIU Qing-jun ZHANG Ming Department of Hepatopancreatobilary Surgery Huzhon Central Hospital Huzhou Zhejiang 313000 China College of Life Science Zhejiang University Hangzhou Zhejiang 310058 China Biosensor National Special Laboratory Department of Biomedical Engineering Zhejiang University Hangzhou Zhejiang 310027 China

Background Embryonic stem （ES） cells poss unlimited self-renewal capacity and the ability to differentiate into cell of all three germ layers in vitro. Induced differentiation of ES cells to neural lineage cells has great potential in basic study of neurogenesis and regeneration therapy of neurodegenerative diseases. histone deacetylase （HDAC） inhibitors enhance histone acetylation so that globularly activate gene expression and may initiate multilineage differentiation. In this study,we aimed to develop a method to induce the differentiation of ES cells to neural cells combining HDAC inhibition and neural cellselection.Methods In this study, we used HDAC inhibitor sodium butyrate （NAB） to induce the differentiation of mouse embryonic stem cells to neural cells through monolayer culture. After differentiation initiation by histone deacetylase inhibitor sodium butyrate, neural cells were induced and selected with a serum free culture system. Results Homogeneous neurons without glial cells demonstrated by molecular marker expression were differentiated with the method. The resultant neurons were excitable. Conclusion The method combined differentiation induction effect of HDAC inhibitors and selective culture system to derive neural cells from ES cells, and implied the involvement of epigenetic regulation in neural differentiation.

关键词： embryonic stem cells histone deacetylase inhibitor neural differentiation adherent monoculture

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histone deacetylase inhibitor pre-treatment enhances the efficacy of DNA-interacting chemotherapeutic drugs in gastric cancer

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World Journal of Gastroenterology 2020年第6期26卷 598-613页

作者： Ramchandra Vigay Amnekar Shafqat Ali Khan Mudasir Rashid Bharat Khade Rahul Thorat Poonam Gera Shailesh V Shrikhande Duane T Smoot Hassan Ashktorab Sanjay Gupta Epigenetics and Chromatin Biology Group Gupta LaboratoryCancer Research InstituteAdvanced Centre for Treatment Research and Education in CancerTata Memorial CentreKhargharNavi MumbaiMaharashtra 410210India Homi Bhabha National Institute Training School ComplexAnushakti NagarMumbaiMaharashtra 400085India Department of Developmental Biology School of MedicineWashington University in St.LouisSaint LouisMO 63130United States Animal House Facility Cancer Research InstituteAdvanced Centre for Treatment Research and Education in CancerTata Memorial CentreKhargharNavi MumbaiMaharashtra 410210India Biorepository Lab Advanced Centre for Treatment Research and Education in CancerTata Memorial CentreKhargharNavi MumbaiMaharashtra 410210India Gastrointestinal and Hepato-Pancreato-Biliary Service Department of Surgical OncologyTata Memorial HospitalParelMumbai 400012India Department of Medicine Meharry Medical CenterNashvilleTN 37208United States Department of Medicine and Cancer Center College of MedicineHoward UniversityWashington DCWA 20060United States

BACKGROUND The prognosis of gastric cancer continues to remain poor,and epigenetic drugs like histone deacetylase inhibitors(HDACi)have been envisaged as potential therapeutic agents.Nevertheless,clinical trials are facing issues with toxicity and efficacy against solid tumors,which may be partly due to the lack of patient stratification for effective treatments.To study the need of patient stratification before HDACi treatment,and the efficacy of pre-treatment of HDACi as a chemotherapeutic drug sensitizer.METHODS The expression activity of class 1 HDACs and histone acetylation was examined in human gastric cancer cells and tissues.The potential combinatorial regime of HDACi and chemotherapy drugs was defined on the basis of observed drug binding assays,chromatin remodeling and cell death.RESULTS In the present study,the data suggest that the differential increase in HDAC activity and the expression of class 1 HDACs are associated with hypoacetylation of histone proteins in tumors compared to normal adjacent mucosa tissue samples of gastric cancer.The data highlights for the first time that pretreatment of HDACi results in an increased amount of DNA-bound drugs associated with enhanced histone acetylation,chromatin relaxation and cell cycle arrest.Fraction-affected plots and combination index-based analysis show that pre-HDACi chemo drug combinatorial regimes,including valproic acid with cisplatin or oxaliplatin and trichostatin A with epirubicin,exhibit synergism with maximum cytotoxic potential due to higher cell death at low combined doses in gastric cancer cell lines.CONCLUSION Expression or activity of class 1 HDACs among gastric cancer patients present an effective approach for patient stratification.Furthermore,HDACi therapy in pretreatment regimes is more effective with chemotherapy drugs,and may aid in predicting individual patient prognosis.

关键词： Chemotherapy Combinatorial index Gastric cancer histone acetylation histone deacetylase inhibitor Patient stratification

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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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Epigenetic reprogramming, gene expression and in vitro development of porcine SCNT embryos are significantly improved by a histone deacetylase inhibitor--- m-carboxycinnamic acid bishydroxamide （CBHA）

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Protein & Cell 2014年第5期5卷 382-393页

作者： Yuran Song Tang Hai Ying Wang Runfa Guo Wei Li Liu Wang Qi Zhou State Key Laboratory of Reproductive Biology Institute of Zoology Chinese Academy of Sciences Beijing 100101 China Graduate University'of the Chinese Academyof Sciences Beijing 100049 China

Insufficient epigenetic reprogramming of donor nuclei is believed to be one of the most important causes of low development efficiency of mammalian somatic cell nuclear transfer （SCNT）. Previous studies have shown that both the in vitro and in vivo development of mouse SCNT embryos could be increased significantly by treat- ment with various histone deacetylase inhibitors （HDACi）, including Trichostatin A, Scriptaid, and m-carboxycin- namic acid bishydroxamide （CBHA）, in which only the effect of CBHA has not yet been tested in other species. In this paper we examine the effect of CBHA treatment on the development of porcine SCNT embryos. We have dis- covered the optimum dosage and time for CBHA treat- ment： incubating SCNT embryos with 2 pmol/L CBHA for 24 h after activation could increase the blastocyst rate from 12.7% to 26.5%. Immunofluorescence results showed that the level of acetylation at histone 3 lysine 9 （AcH3K9）, acetylation at histone 3 lysine 18 （AcH3K18）, and acetylation at histone 4 lysine 16 （AcH4K16） was raised after CBHA treatment. Meanwhile, CBHA treatment improved the expression of development relating genes such as pou5fl, cdx2, and the imprinted genes like igf2. Despite these promising in vitro results and histone reprogramming, the full term development was notsignificantly increased after treatment. In conclusion, CBHA improves the in vitro development of pig SCNT embryos, increases the global histone acetylation and corrects the expression of some developmentally important genes at early stages. As in mouse SCNT, we have shown that nuclear epigenetic reprogramming in pig early SCNT embryos can be modified by CBHA treatment.

关键词： swine nuclear transfer epigeneticreprogramming histone deacetylase inhibitor

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inhibitory Effect of histone deacetylase inhibitor on the Proliferation of Leukemia Cells and Its Anti-Tumor Pharmacology

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Journal of Biosciences and Medicines 2021年第1期9卷 30-40页

作者： Shubo Wang College of Pharmacy Jinan University Guangzhou China

The aim of this study was to explore the inhibitory effect of histone deacetylase inhibitor (HDACI) on the proliferation of leukemia cells. The two kinds of leukemia cells (human promyelocytic leukemia cell (HL-60) and human acute myelogenous leukemia cell (KG-1)) were selected for in vitro research. Besides, Chidamide, a kind of benzamide HDACI, was applied to induce and culture the HL-60 and KG-1 cells, and the anti-tumor cell proliferation activity of Chidamide on HL-60 and KG-1 was detected by the methyl thiazolyl tetrazolium (MTT) assay, which was 5.6 and 6.1 in turn. The cell scratch experiment verified that Chidamide had the metastasis inhibitory effect on HL-60 and KG-1 cells. Flow cytometry was employed to measure the percentage of apoptotic cells, and it was found that the percentage of apoptotic cells was 55.6% ± 1% and 48.6% ± 1% in sequence after HL-60 and KG-1 cells were treated with Chidamide for 36 hours. The number of auto-phagosomes was determined by transmission electron microscopy showing that the number of auto-phagosomes in HL-60 and KG-1 cells was 12 ± 1 and 10 ± 1, respectively after the induction process of Chidamide. The phosphorylated histone H2AX protein (γ-H2AX) recognition antibody immunofluorescence method was adopted to determine the deoxyribonucleic acid (DNA) damage, and the positive rates of HL-60 and KG-1 cells reached 28.41% and 26.35%, respectively after Chidamide treatment. Therefore, Chidamide, as a kind of HDACI, could effectively inhibit the proliferation of leukemia cells, so that the results of this experiment had a good guiding meaning for the clinical diagnosis and treatment of leukemia.

关键词： Tumor Cell Proliferation histone deacetylase inhibitor Chidamide Leukemia Treatment

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The histone deacetylase inhibitor valproic acid（VPA） inhibits proliferation and induces apoptosis in gastric cancer

The histone deacetylase inhibitor valproic acid（VPA） inhib...

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2017年中国肿瘤标志物学术大会暨第十一届肿瘤标志物青...

作者： Jie Sun Tiefeng Jin Zhenhua Lin Department of Pathology ＆ Cancer Research Center Yanbian University Medical College

Objectives: To investigate the therapeutic potential of VPA against gastric adenocarcinoma, and explore the related mechanisms.Materials and methods: Gastric cancer cell lines AGS, MKN-28, MKN-74, SGC-7901 proliferation treated by VPA was detected by MTT. Colony formation and Western blot assays were used to screen for the proliferation attenuating effects of VPA on gastric cancer cells AGS and SGC-7901. Annexin-V/PI double staining flow cytometry and hoechst staining assays were used to detect the apoptosis of AGS and SGC-7901 cells after the treatment with VPA. Western blot assays were performed to analyse the activation of caspases and apoptosis-related protein expression. To investigate the mechanisms underlying the inhibition of cell growth by VPA, western blot assays were performed to detect the expression of PI3 K/AKT/mTOR signaling pathway in AGS and SGC-7901 cells treated by VPA.Results: The MTT assays showed that the inhibition of cell growth in gastric cancer cells AGS, MKN-28, MKN-74, SGC-7901 were dependent on the dose of VPA. AGS and SGC-7901 cells exhibited the most sensitivity towards VPA in growth inhibition. Colony formation and western blot assays were observed the anti–proliferative potential of VPA on gastric cancer cells. Hoechst33342 staining showed that more frequency chromatin fragmentation and condensation in AGS and SGC-7901 cells exposed to concomitant treatment compared with the control group. Flow cytometry results of VPA-treated gastric cancer cells confirmed the augment of apoptosis. Western blot results showed that VPA could activate caspase-3, caspase-8, caspase-9 and induce apoptosis. As to the mechanisms, increased expression of PTEN and decreased p-AKT, p-S6, p-mTOR and p-4 EBP1 expressions were observed in AGS and SGC-7901 cells after VPA treatment. Conclusions: VPA inhibits the proliferation of gastric adenocarcinoma cells via the modulation of apoptosis and contributes to its cytotoxicity against gastric adenocarcinoma involving the inhibition of PI3 K/AKT/mTOR signaling pa

关键词： histone deacetylase inhibitor valproic acid gastric adenocarcinoma apoptosis

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Chidamide and sintilimab combination in diffuse large B-cell lymphoma progressing after chimeric antigen receptor T therapy

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World Journal of Clinical Cases 2022年第19期10卷 6555-6562页

作者： Yuan-Yuan Hao Pan-Pan Chen Xiang-Gui Yuan Ai-Qi Zhao Yun Liang Hui Liu Wen-Bin Qian Department of Hematology The Second Affiliated Hospital of Zhejiang University School of MedicineHangzhou 310009Zhejiang ProvinceChina

BACKGROUND Diffuse large B-cell lymphoma(DLBCL)is curable with first-line chemoimmunotherapy but patients with relapsed/refractory(R/R)DLBCL still face a poor prognosis.For patients with R/R DLBCL,the complete response rate to traditional next-line therapy is only 7%and the median overall survival is 6.3 mo.Recently,CD19-targeting chimeric antigen receptor T cells(CAR-T)have shown promise in clinical trials.However,approximately 50%of patients treated with CAR-T cells ultimately progress and few salvage therapies are effective.CASE SUMMARY Here,we report on 7 patients with R/R DLBCL whose disease progressed after CAR-T infusion.They received a PD-1 inhibitor(sintilimab)and a histone deacetylase inhibitor(chidamide).Five of the 7 patients tolerated the treatment without any serious adverse events.Two patients discontinued the treatment due to lung infection and rash.At the 20-mo follow-up,the median overall survival of these 7 patients was 6 mo.Of note,there were 2 complete response rates(CRs)and 2 partial response rates(PRs)during this novel therapy,with an overall response rate(ORR)of 57.1%,and one patient had a durable CR that lasted at least 20 mo.CONCLUSION In conclusion,chidamide combined with sintilimab may be a choice for DLBCL patients progressing after CD19-targeting CAR-T therapy.

关键词： Chimeric antigen receptor T cell therapy Diffuse large B-cell lymphoma Immunotherapy PD-1 inhibitor histone deacetylase inhibitor Case report

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Chidamide,Decitabine,Cytarabine,Aclarubicin,and Granulocyte Colony-stimulating Factor Therapy for Patients with Relapsed/Refractory Acute Myeloid Leukemia:A Retrospective Study from a Single-Center

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Current Medical Science 2023年第6期43卷 1151-1161页

作者： Fan-cong KONG Ling QI Yu-lan ZHOU Min YU Wen-feng HUANG Fei LI Center of Hematology The First Affiliated Hospital of Nanchang UniversityNanchang330006China Jiangxi Clinical Research Center for Hematologic Diseases Nanchang330006China

Objective Preclinical evidence and clinical trials have suggested synergistic effects of epigenetic modifiers in combination with cytotoxic agents for the treatment of leukemia.However,their efficacy in patients with relapsed/refractory acute myeloid leukemia(R/R AML)remains unclear.Methods Clinical data of R/R AML patients who received a CDCAG regimen(chidamide,decitabine,cytarabine,aclarubicin,and granulocyte colony-stimulating factor)from July 1,2018 to October 31,2021 at our center were retrospectively assessed,and the safety and efficacy of the CDCAG regimen were evaluated.Patients were followed up until November 30,2021,with a median follow-up of 21.6 months(95%CI:10.0–33.2 months).Results A total of 67 patients were enrolled.Two patients died within 3 weeks after the initiation,and therefore only 65 patients underwent the assement for clinical response and survival.It was found that 56.9%patients achieved complete remission with a median overall survival(OS)of 9.6 months.The median OS of responders was 25.9 months,while that of non-responders was 5.0 months(P<0.0001).Patients with gene mutations had a superior overall response rate(ORR)(80.4%vs.45.5%,P=0.043)compared to those without gene mutations.The presence of DNA methyltransferase 3 A(DNMT3A),ten-eleven translocation-2(TET2),and isocitrate dehydrogenase 1/2(IDH1/2)mutations did not affect the response rate(88.2%vs.68.9%,P=0.220)and reflected a better OS(not attained vs.9.0 months,P=0.05).The most common non-hematologic adverse events were pulmonary infection(73.1%),followed by febrile neutropenia(23.9%)and sepsis(19.4%).Conclusions The CDCAG regimen was effective and well-tolerated in R/R AML patients,increasing the potential for allogeneic hematopoietic stem cell transplantation.Moreover,patients with DNMT3A,TET2,and IDH1/2 mutations might benefit from this regimen.

关键词： relapsed/refractory acute myeloid leukemia histone deacetylase inhibitor DNA methyltransferase inhibitor salvage therapy

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histone deacetylase inhibitors Romidepsin and Vorinostat Promote Hepatitis B Virus Replication by Inducing Cell Cycle Arrest

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Journal of Clinical and Translational Hepatology 2021年第2期9卷 160-168页

作者： Yang Yang Yu Yan Zhen Chen Jie Hu Kai Wang Ni Tang Xiaosong Li Zhi Zhou Key Laboratory of Molecular Biology for Infectious Diseases(Ministry of Education) Institute for Viral HepatitisDepartment of Infectious DiseasesThe Second Affiliated HospitalChongqing Medical UniversityChongqingChina Clinical Molecular Medicine Testing Center The First Affiliated HospitalChongqing Medical UniversityChongqingChina Department of Infectious Diseases The Second Affiliated HospitalChongqing Medical UniversityChongqingChina

Background and Aims:Chronic hepatitis B virus(HBV)infection is a global public health challenge.HBV reactivation usually occurs in cancer patients after receiving cytotoxic chemotherapy or immunosuppressive therapies.Romidepsin(FK228)and vorinostat(SAHA)are histone deacetylase inhibitors(HDACi)approved by the Food and Drug Administration as novel antitumor agents.The aim of this study was to explore the effects and mechanisms of HDACi treatment on HBV replication.Methods:To assess these effects,human hepatoma cell lines were cultured and cell viability after FK228 or SAHA treatment was measured by the CCK-8 cell counting kit-8 assay.Then,HBV DNA and RNA were quantified by real-time PCR and Southern blotting.Furthermore,analysis by western blotting,enzyme-linked immunosorbent assay(ELISA),immunohistochemistry,and flow cytometry was performed.Results:FK228/SAHA treatment significantly promoted HBV replication and biosynthesis in both HBV-replicating cells and HBV-transgenic mouse model.Flow cytometry assay indicated that FK228/SAHA enhanced HBV replication by inducing cell cycle arrest through modulating the expression of cell cycle regulatory proteins.In addition,simultaneous inhibition of HDAC1/2 by FK228 promoted HBV replication more effectively than the broad spectrum HDAC inhibitor SAHA.Conclusions:Overall,our results demonstrate that cell cycle blockage plays an important role in FK228/SAHAenhanced HBV replication,thus providing a potential avenue for rational use of HDACi in patients with chronic hepatitis B.

关键词： HBV reactivation histone deacetylase inhibitor Romidepsin Vorinostat Cell cycle

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Trichostatin A Extends the Lifespan of Drosophila melanogaster by Elevating hsp22 Expression

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Acta Biochimica et Biophysica Sinica 2004年第9期36卷 618-622页

作者： Dan TAO#, Jun LU#, Hui SUN, Yan-Mei ZHAO, Zhi-Gen YUAN, Xiao-Xue LI, and 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 level of acetylation of histones in nucleosomes is related to the longevity of yeast and animals. However, the mechanisms by which acetylation and deacetylation affect longevity remain unclear. In present study, we investigated the influence of histone acetylation modification on the expression of hsp22 gene and the lifespan in Drosophila melanogaster using histone deacetylase (HDAC) inhibitor Trichostatin A (TSA). The results showed that TSA could extend the lifespan of Drosophila melanogaster. Furthermore, TSA significantly promoted the hsp22 gene transcription, and affected the chromatin morphology at the locus of hsp22 gene along the polytene chromosome. Present data implicate that TSA may affect the lifespan of Drosophila through changing the level of histone acetylation and influencing the expression of hsp22 gene that is related to aging.

关键词： histone acetylation histone deacetylase inhibitor Drosophila melanogaster hsp22 lifespan

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