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Asian Pacific Journal of Tropical Biomedicine 2024年第2期14卷 65-72,I0002-I0005页

作者： Ye-eun Kim Jeonghye Hwang Ki-Young Kim Graduate School of Biotechnology Kyung Hee UniversitySeocheonGiheungYonginGyeonggi-do 446-701Republic of Korea Department of Genetics and Biotechnology College of Life SciencesKyung Hee UniversitySeocheonGiheungYonginGyeonggi-do 446-701Republic of Korea

Objective:To examine the inhibitory effect of Hydrangea serrata extract against hepatocellular carcinoma HepG2 cells and its underlying mechanisms.Methods:The effects of Hydrangea serrata extract on growth inhibition of tumor cells and spheroids were assessed using MTT and 3D culture assays.Quantitative real-time PCR and Western blot analyses were employed to investigate the changes in mRNA and protein expression levels of molecules related to cell cycle and apoptosis.Results:Hydrangea serrata extract effectively inhibited the growth of both tumor cells and spheroids.The extract also significantly upregulated p27 mRNA expression and downregulated CDK2 mRNA expression,leading to cell cycle arrest.Moreover,increased BAX/Bcl-2 ratio as well as caspase-9 and-3 were observed after treatment with Hydrangea serrata extract,indicating the induction of tumor cell apoptosis.Conclusions:Hydrangea serrata extract has the potential to alleviate tumors by effectively modulating cell-cycle-related gene expressions and inducing apoptosis,thereby inhibiting tumor growth.

关键词： Hydrangea serrata Hepatocellular carcinoma Liver cancer Anticancer cell cycle arrest Apoptosis

Antitumor Effect of Apcin on Endometrial Carcinoma via p21-Mediated cell cycle arrest and Apoptosis

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Current Medical Science 2024年第3期44卷 623-632页

作者： Ke NI Zi-li LI Zhi-yong HU Li HONG Department of Obstetrics and Gynecology Renmin Hospital of Wuhan UniversityWuhan430060China Institute of Reproductive Health Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China

Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential target is cell division cycle 20(CDC20),which has been implicated in oncogenesis.This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved.Methods The effects of Apcin on EC cell proliferation,apoptosis,and the cell cycle were evaluated using CCK8 assays and flow cytometry.RNA sequencing(RNA-seq)was subsequently conducted to explore the underlying molecular mechanism,and Western blotting and coimmunoprecipitation were subsequently performed to validate the results.Animal studies were performed to evaluate the antitumor effects in vivo.Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC.Results Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells,resulting in cell cycle arrest.Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin.Notably,Apcin treatment led to the upregulation of the cell cycle regulator p21,which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells.In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth.Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue,and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval.Conclusion CDC20 is a novel molecular target in EC,and Apcin could be developed as a candidate antitumor drug for EC treatment.

关键词： endometrial carcinoma CDC20 apoptosis cell cycle arrest p21 BBC3

Combinatorial effect of diclofenac with piperine and D-limonene on inducing apoptosis and cell cycle arrest of breast cancer cells

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Asian Pacific Journal of Tropical Biomedicine 2023年第2期13卷 80-92页

作者： Srivarshini Sankar Gothandam Kodiveri Muthukaliannan School of Bio Sciences and Technology Vellore Institute of TechnologyVelloreTamil NaduIndia

Objective:To investigate the potential synergistic activity of diclofenac with piperine and D-limonene in inducing apoptosis and cell cycle arrest in breast cancer MCF-7 cells.Methods:Molecular docking study was conducted to evaluate the binding affinity of diclofenac with piperine and D-limonene against p53,Bax,and Bcl-2.The MTT assay was used to determine IC50,and the Chou-Talay method was used to determine the synergistic concentration of the combination treatment of diclofenac plus piperine and diclofenac plus D-limonene.Apoptosis detection,cell cycle arrest,reactive oxygen species production,and mitochondrial membrane potential were also investigated.Results:Diclofenac,piperine,and D-limonene showed potent binding affinity for p53,Bax,and Bcl-2.Diclofenac plus piperine and diclofenac plus D-limonene enhanced the formation of reactive oxygen species,which also had an effect on the mitochondrial membrane’s integrity and caused DNA fragmentation.Diclofenac plus piperine and diclofenac plus D-limonene arrested the cells in the sub-G0phase while drastically lowering the percentage of cells in the G2/M phase.Furthermore,the elevated apoptosis in the combined therapy was confirmed by annexin V/propidium iodide staining.Conclusions:The combined therapy prominently enhanced the antiproliferative and apoptotic effects on MCF-7 cells compared with treatment with diclofenac,piperine,and D-limonene alone.

关键词： Breast cancer Diclofenac sodium Piperine D-limonene Reactive oxygen species cell cycle arrest Apoptosis

Marsdenia tenacissima extract induces G_0/G_1 cell cycle arrest in human esophageal carcinoma cells by inhibiting mitogen-activated protein kinase(MAPK) signaling pathway

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Chinese Journal of Natural Medicines 2015年第6期13卷 428-437页

作者： FAN Wei SUN Li ZHOU Jing-Qian ZHANG Cang QIN Song TANG Ying LIU Yang LIN Sen-Sen YUAN Sheng-Tao Jiangsu Center for Drug Screening China Pharmaceutical University Department of Complex Prescription of Traditional Chinese Medicine School of Chinese Material Medicine China Pharmaceutical University Nanjing Sanhome Pharmaceutical Co. Ltd. Jiangsu Center for Pharmacodynamics Research and Evaluation China Pharmaceutical University

Marsdenia tenacissima extract(MTE, trade name: Xiao-Ai-Ping injection) is an extract of a single Chinese plant medicine. It has been used for the treatment of cancer in China for decades, especially for esophageal cancer and other cancers in the digestive tract. In the present study, the potential mechanism for MTE's activity in esophageal cancer was explored. The effects of MTE on the proliferation of human esophageal cancer cells(KYSE150 and Eca-109) were investigated by the MTT assay, the Brd U(bromodeoxyuridine) incorporation immunofluorescence assay, and flow cytometric analysis. MTE inhibited cell proliferation through inducing G0/G1 cell cycle arrest in KYSE150 and Eca-109. Western blot analysis was employed to determine protein levels in the MTE treated cells. Compared with the control cells, the expression levels of the cell cycle regulatory proteins cyclin D1/D2/D3, cyclin E1, CDK2/4/6(CDK: cyclin dependent kinase), and p-Rb were decreased significantly in the cells treated with MTE at 40 mg·m L-1. In addition, MTE had an inhibitory effect on the MAPK(mitogen-activated protein kinase) signal transduction pathway, including ERK(extracellular signal-regulated kinase), JNK(c-Jun N-terminal kinase), and p38 MAPK. Moreover, MTE showed little additional effects on the regulation of cyclin D1/D3, CDK4/6, and p-Rb when the ERK pathway was already inhibited by the specific ERK inhibitor U0126. In conclusion, these data suggest that MTE inhibits human esophageal cancer cell proliferation through regulation of cell cycle regulatory proteins and the MAPK signaling pathways, which is probably mediated by the inhibition of ERK activation.

关键词： Marsdenia tenacissima extract cell cycle arrest Mitogen-activated protein kinase signaling pathway Human esophageal cancer

Silibinin induces hepatic stellate cell cycle arrest via enhancing p53/p27 and inhibiting Akt downstream signaling protein expression

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Hepatobiliary & Pancreatic Diseases International 2017年第1期16卷 80-87页

作者： Devaraj Ezhilarasan Jonathan Evraerts Brice Sid Pedro Buc Calderon Sivanesan Karthikeyan Etienne Sokal Mustapha Najimi institut de recherche expérimentale et clinique (irec) laboratory of pediatric hepatology and cell therapyuniversité catholique de louvain 1200 Brussels Belgium louvain drug research institute toxicology and cancer biology research group pmnt unituniversité catholique de louvain 1200 Brussels Belgium facultad de ciencias de la salud universidad arturo prat Iquique Chil department of pharmacology and environmental toxicology food and hepatotoxicology laboratory dr. alm post graduate institute of basic medical sciences university of madrastaramani campus Chennai-600 l13 India

BACKGROUND： Proliferation of hepatic stellate cells （HSCs） plays a pivotal role in the progression of liver fibrosis conse- quent to chronic liver injury. Silibinin, a flavonoid compound, has been shown to possess anti-fibrogenic effects in animal models of liver fibrosis. This was attributed to an inhibition of cell proliferation of activated HSCs. The present study was to gain insight into the molecular pathways involved in silibinin anti-fibrogenic effect. METHODS： The study was conducted on LX-2 human stellate cells treated with three concentrations of silibinin （10, 50 and 100 μmol/L） for 24 and 96 hours. At the end of the treatment cell viability and proliferation were evaluated. Protein expression of p27, p21, p53, Akt and phosphorylated-Akt was evaluated by Western blotting analysis and Ki-67 protein expression was by immunocytochemistry. Sirtuin activity was evaluated by chemiluminescence based assay. RESULTS： Silibinin inhibits LX-2 cell proliferation in doseand time-dependent manner; we showed that silibinin upregulated the protein expressions of p27 and p53. Such regulation was correlated to an inhibition of both downstream Akt and phosphorylated-Akt protein signaling and Ki-67 protein expression. Sirtuin activity also was correlated to silibinin- inhibited proliferation of LX-2 cells. CONCLUSION： The anti-proliferative effect of silibinin on LX-2 human steUate cells is via the inhibition of the expres- sions of various cell cycle targets including p27, Akt and sir- tuin signaling.

关键词： silibinin hepatic stellate cells in vitro cell cycle arrest proliferation

Carbon ion irradiation-induced DNA damage evokes cell cycle arrest and apoptosis via the pRb/E2F1/c-Myc signaling pathway in p53-deficient prostate cancer PC-3 cells

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Nuclear Science and Techniques 2021年第3期32卷 82-93页

作者： Fang Wang Yi Xiao Jun-Fang Yan Guo-Min Huang Jin-Hua Zhang Cui-Xia Di Jing Si Hong Zhang Ai-Hong Mao Institute of Modern Physics Chinese Academy of SciencesLanzhou 730000China School of Life Science and Engineering Lanzhou University of TechnologyLanzhou 730050China Department of Mammary Gland the First Hospital of Lanzhou UniversityLanzhou 730000China University of Chinese Academy of Sciences Beijing 100039China Gansu Provincial Academic Institute for Medical Research Lanzhou 730050China

Carbon ion radiotherapy has the advantages of better therapeutic effect and fewer side effects compared with those of X-rays in many kinds of tumors,including prostate cancer,and thus is an attractive treatment approach for prostate cancer.However,the biological effects and underlying mechanisms of carbon ion irradiation in prostate cancer are not yet fully understood.Therefore,this study systematically compared the effects of carbon ion irradiation with those of X-ray irradiation on DNA damage response and found that carbon ion irradiation was more effective than X-ray irradiation.Carbon ion irradiation can induce a high level of DNA double-strand break damage,reflected by the number of y-H2 A histone family member X foci,as well as by the foci lasting time and size.Moreover,carbon ion irradiation exhibited strong and long-lasting inhibitory effect on cell survival capability,induced prolonged cell cycle arrest,and increased apoptosis in PC-3 cells.As an underlying mechanism,we speculated that carbon ion irradiation-induced DNA damage evokes cell cycle arrest and apoptosis via the pRb/E2 F1/c-Myc signaling pathway to enhance the radiosensitivity of p53-deficient prostate cancer PC-3 cells.Collectively,the present study suggests that carbon ion irradiation is more efficient than X-ray irradiation and may help to understand the effects of different radiation qualities on the survival potential of p53-deficient prostate cancer cells.

关键词： Carbon ion irradiation DNA damage cell cycle arrest Apoptosis C-Myc Prostate cancer

cell cycle arrest, Apoptosis, and Autophagy Induced by chabamide in Human Leukemia cells

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Chinese Herbal Medicines 2016年第1期8卷 30-38页

作者： Kun Hu Meng Yang Yuan-yuan Xu Kun Wei Jie Ren School of Pharmaceutical Engineering & Life Science Changzhou University Key Laboratory of Medicinal Chemistry for Natural Resource (Yunnan University) Ministry of Education School of Chemical Science and Technology Yunnan University

Objective To investigate the antitumor effect of chabamide in K562 （human leukemia cell line） cells. Methods The cytotoxicity was assessed by a standard colorimetric assay using 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT）. The morphological changes were observed by Hoechst 33258 staining. Induction of apoptosis, loss of the mitochondrial membrane potential （A ~＇m）, and cell cycle analysis were evaluated by flow cytometry （FCM） analysis. Levels of apoptosis-related proteins, ceil cycle-related proteins, and LC3 protein were detected by Western blotting. Moreover, the autophagy induced by chabamide was also detected by MDC fluorescent staining. Results Chabamide significantly inhibited cell proliferation by cell cycle arrest in the Go/G1 phase. This phenomenon was associated with an obvious increase in p21 expression and decrease in cyclin D1 and cyclin-dependent kinase 2/4/6 protein expression. Moreover, chabamide could regulate the changes in mitochondrial membrane potential, increase the expression of apoptosis-related proteins, such as Bax and cytochrome C, and decrease the protein expression of Bcl-2, caspase-9, caspase-3, and PARP-1. JNK, ERK1/2, and p38 were also regulated by chabamide in K562 cells. Furthermore, induction of autophagy, marked by autophagic vacuole formation, was detected. Conversion of LC3-1 to LC3-11, a marker of active autophagosome formation, was also detected following chabamide treatment. Conclusion The antitumor activity of chabamide with the results of apoptosis and autophagy induction was confirmed in K562 cells.

关键词： apoptosis autophagy chabamide cell cycle arrest MAPKs

The MORC2 p.S87L mutation reduces proliferation of pluripotent stem cells derived from a patient with the spinal muscular atrophy-like phenotype by inhibiting proliferation-related signaling pathways

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Neural Regeneration Research 2024年第1期19卷 205-211页

作者： Sen Zeng Honglan Yang Binghao Wang Yongzhi Xie Ke Xu Lei Liu Wanqian Cao Xionghao Liu Beisha Tang Mujun Liu Ruxu Zhang Department of Neurology The Third Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Department of Radiology The Third Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Health Management Center The Third Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Center for Medical Genetics&Hunan Key Laboratory of Medical Genetics School of Life SciencesCentral South UniversityChangshaHunan ProvinceChina National Clinical Research Center for Geriatric Disorders Central South UniversityChangshaHunan ProvinceChina Department of cell Biology School of Life SciencesCentral South UniversityChangshaHunan ProvinceChina

Mutations in the microrchidia CW-type zinc finger protein 2(MORC2)gene are the causative agent of Charcot-Marie-Tooth disease type 2Z(CMT2Z),and the hotspot mutation p.S87L is associated with a more seve re spinal muscular atrophy-like clinical phenotype.The aims of this study were to determine the mechanism of the severe phenotype caused by the MORC2 p.S87L mutation and to explore potential treatment strategies.Epithelial cells were isolated from urine samples from a spinal muscular atrophy(SMA)-like patient[MORC2 p.S87L),a CMT2Z patient[MORC2 p.Q400R),and a healthy control and induced to generate pluripotent stem cells,which were then differentiated into motor neuron precursor cells.Next-generation RNA sequencing followed by KEGG pathway enrichment analysis revealed that differentially expressed genes involved in the PI3K/Akt and MAP K/ERK signaling pathways were enriched in the p.S87L SMA-like patient group and were significantly downregulated in induced pluripotent stem cells.Reduced proliferation was observed in the induced pluripotent stem cells and motor neuron precursor cells derived from the p.S87L SMA-like patient group compared with the CMT2Z patient group and the healthy control.G0/G1 phase cell cycle arrest was observed in induced pluripotent stem cells derived from the p.S87L SMA-like patient.MORC2 p.S87Lspecific antisense oligonucleotides(p.S87L-ASO-targeting)showed significant efficacy in improving cell prolife ration and activating the PI3K/Akt and MAP K/ERK pathways in induced pluripotent stem cells.Howeve r,p.S87L-ASO-ta rgeting did not rescue prolife ration of motor neuron precursor cells.These findings suggest that downregulation of the PI3K/Akt and MAP K/ERK signaling pathways leading to reduced cell proliferation and G0/G1 phase cell cycle arrest in induced pluripotent stem cells might be the underlying mechanism of the severe p.S87L SMA-like phenotype.p.S87L-ASO-targeting treatment can alleviate disordered cell proliferation in the early stage of pluripotent stem cell induction.

关键词： antisense oligonucleotides cell cycle arrest Charcot-Marie-Tooth disease 2Z induced pluripotent stem cells MAPK/ERK PI3K/Akt proliferation spinal muscular atrophy-like

ZMYND10 downregulates cyclins B1 and D1 to arrest cell cycle by trimethylating lysine 9 on histone 3

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Life Research 2021年第4期4卷 17-24页

作者： Long-Ji Wu Xiang-Ning Zhang Jian Wang Xia Kong Bi-Ying Zheng Jing Huang Hong-Bing Yu Zhi-Wei He Department of Pathophysiology School of Basic Medical ScienceGuangdong Medical UniversityDongguanGuangdongChina Chinese-American Tumor Institute Guangdong Provincial Key Laboratory of Medical DiagnosticsGuangdongChina. Department of Clinical Microbiology Institute of Laboratory MedicineGuangdong Medical UniversityDongguanGuangdongChina.

The BLU gene coding for zinc finger,MYND-type containing 10(ZMYND10)protein is mapped on chromosomal region 3p21.It is frequently lost in some kinds of cancers due to hypermethylation on its promoter region and identified as a tumour suppressor gene.The underlying mechanisms for BLU-mediated tumor suppression remain unclear.BLU has been reported to disturb cell cycle progression.The present study aims at examining whether ZMYND10 prevents progression of the cell cycle by targeting to repressive histone marks and downregulating the level of cyclins.Proteins structurally similar with ZMYND10 have been shown to recognize DNA sequence upstream of coding portion of the gene encoding cell cycle regulators.Enzymes,notably demethylases modifying the lysine residues are over-expressed line oncoproteins,and targeted in anti-cancer therapy.BLU was re-expressed in H1299 and HepG2 cells.The level of cyclin D1,cyclin B1 and trimethylate lysine 9 on histone 3(H3K9me3)and the binding of BLU with SIN3A(a component of the co-repressor)were detected.cell cycle profile was measured.The evolutionary relationship between ZMYND10 and other ZMYND proteins was analysed by phylogenetic tree construction.We found that BLU expression induced G1 arrest in H1299 cells,and induced G1/G2 arrest in HepG2 cells.cell cycle arrest was correlated with reduced activities and levels of cyclins;cyclin D1 was downregulated in H1299 cells;Both cyclin B1 and D1 were downregulated in HepG2 cells;and that BLU was associated with SIN3A.In both cell lines,the expression of H3K9me3 was induced.BLU was clustered with histone methyltransferase SMYD3 and SMYD1 on the same clade of the deduced phylogenetic tree.The results thus suggested that ZMYND10 encoded by BLU inhibited cyclins activity to prevent cell cycle progression through interaction with repressors and histone repressive marks to block the expression of genes coding for cyclins.

关键词： BLU/ZMYND10 tumor suppression cell cycle arrest cyclin trimethylated lysine 9 on histone 3

T63,A 4-Arylidene Curcumin Analogue induces cell cycle arrest and apoptosis through activation of FOXO3a transcription factors

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T63,A 4-Arylidene Curcumin Analogue induces cell cycle arres...