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Melatonin improves the first cleavage of parthenogenetic embryos from vitrified-warmed mouse oocytes potentially by promoting cell cycle progression

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Journal of Animal Science and Biotechnology 2022年第1期13卷 106-122页

作者： Bo Pan Izhar Hyder Qazi Shichao Guo Jingyu Yang Jianpeng Qin Tianyi Lv Shengqin Zang Yan Zhang Changjun Zeng Qingyong Meng Hongbing Han Guangbin Zhou Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province College of Animal Science and TechnologySichuan Agricultural UniversityChengdu 611130China Department of Veterinary Anatomy and Histology Shaheed Benazir Bhutto University of Veterinary and Animal SciencesSakrandSindh 67210Pakistan State Key Laboratory of AgroBiotechnology China Agricultural UniversityBeijing 100193China National Engineering Laboratory for Animal Breeding Key Laboratory of Animal Genetics and Breeding of the Ministry of AgricultureBeijing Key Laboratory for Animal Genetic ImprovementCollege of Animal Science and TechnologyChina Agricultural UniversityBeijing 100193China

Background:This study investigated the effect of melatonin(MT)on cell cycle(G1/S/G2/M)of parthenogenetic zygotes developed from vitrified-warmed mouse metaphase II(MII)oocytes and elucidated the potential mechanism of MT action in the first cleavage of embryos.Results:After vitrification and warming,oocytes were parthenogenetically activated(PA)and in vitro cultured(IVC).Then the spindle morphology and chromosome segregation in oocytes,the maternal mRNA levels of genes including Miss,Doc1r,Setd2 and Ythdf2 in activated oocytes,pronuclear formation,the S phase duration in zygotes,mitochondrial function at G1 phase,reactive oxygen species(ROS)level at S phase,DNA damage at G2 phase,early apoptosis in 2-cell embryos,cleavage and blastocyst formation rates were evaluated.The results indicated that the vitrification/warming procedures led to following perturbations 1)spindle abnormalities and chromosome misalignment,alteration of maternal mRNAs and delay in pronucleus formation,2)decreased mitochondrial membrane potential(MMP)and lower adenosine triphosphate(ATP)levels,increased ROS production and DNA damage,G1/S and S/G2 phase transition delay,and delayed first cleavage,and 3)increased early apoptosis and lower levels of cleavage and blastocyst formation.Our results further revealed that such negative impacts of oocyte cryopreservation could be alleviated by supplementation of warming,recovery,PA and IVC media with 10^(−9) mol/L MT before the embryos moved into the 2-cell stage of development.Conclusions:MT might promote cell cycle progression via regulation of MMP,ATP,ROS and maternal mRNA levels,potentially increasing the first cleavage of parthenogenetic zygotes developed from vitrified-warmed mouse oocytes and their subsequent development.

关键词： cell cycle Cleavage rate Melatonin MetaphaseⅡoocyte Parthenogenetic activation Vitrification

CUDC-101 as a dual-target inhibitor of EGFR and HDAC enhances the anti-myeloma effects of bortezomib by regulating G2/M cell cycle arrest

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第5期24卷 442-454页

作者： Wen CAO Shunnan YAO Anqi LI Haoguang CHEN Enfan ZHANG Liqin CAO Jinna ZHANG Yifan HOU Zhenfeng DAI Jing CHEN Xi HUANG Li YANG Zhen CAI Bone Marrow Transplantation Center the First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310006China Institute of Hematology Zhejiang UniversityHangzhou 310058China School of Medicine Zhejiang UniversityHangzhou 310058China

CUDC-101,an effective and multi-target inhibitor of epidermal growth factor receptor(EGFR),histone deacetylase(HDAC),and human epidermal growth factor receptor 2(HER2),has been reported to inhibit many kinds of cancers,such as acute promyelocytic leukemia and non-Hodgkin's lymphoma.However,no studies have yet investigated whether CUDC-101 is effective against myeloma.Herein,we proved that CUDC-101 effectively inhibits the proliferation of multiple myeloma(MM)cell lines and induces cell apoptosis in a time-and dose-dependent manner.Moreover,CUDC-101 markedly blocked the signaling pathway of EGFR/phosphoinositide-3-kinase(PI3K)and HDAC,and regulated the cell cycle G2/M arrest.Moreover,we revealed through in vivo experiment that CUDC-101 is a potent anti-myeloma drug.Bortezomib is one of the important drugs in MM treatment,and we investigated whether CUDC-101 has a synergistic or additive effect with bortezomib.The results showed that this drug combination had a synergistic anti-myeloma effect by inducing G2/M phase blockade.Collectively,our findings revealed that CUDC-101 could act on its own or in conjunction with bortezomib,which provides insights into exploring new strategies for MM treatment.

关键词： CUDC-101 Multiple myeloma Bortezomib Epidermal growth factor receptor(EGFR) cell cycle

Antrodia cinnamomea exerts an anti-hepatoma effect by targeting PI3K/AKT-mediated cell cycle progression in vitro and in vivo

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Acta Pharmaceutica Sinica B 2022年第2期12卷 890-906页

作者： Yan Zhang Pin Lv Junmei Ma Ning Chen Huishan Guo Yan Chen Xiaoruo Gan Rong Wang Xuqiang Liu Sufang Fan Bin Cong Wenyi Kang Hebei Key Laboratory of Forensic Medicine College of Forensic MedicineHebei Medical UniversityShijiazhuang 050017China Hebei Food Safety Key Laboratory Hebei Food Inspection and Research InstituteShijiazhuang 050091China Cardiovascular Medical Science Center Department of Cell BiologyHebei Medical UniversityShijiazhuang 050017China National R&D Center for Edible Fungus Processing Technology Henan UniversityKaifeng 475004China Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology Chinese Academy of Medical SciencesBeijing 100730China

Antrodia cinnamomea is extensively used as a traditional medicine to prevention and treatment of liver cancer.However,its comprehensive chemical fingerprint is uncertain,and the mechanisms,especially the potential therapeutic target for anti-hepatocellular carcinoma(HCC)are still unclear.Using UPLC-Q-TOF/MS,139 chemical components were identified in A.cinnamomea dropping pills(ACDPs).Based on these chemical components,network pharmacology demonstrated that the targets of active components were significantly enriched in the pathways in cancer,which were closely related with cell proliferation regulation.Next,HCC data was downloaded from Gene Expression Omnibus database(GEO).The Cancer Genome Atlas(TCGA)and Dis Ge NET were analyzed by bioinformatics,and 79 biomarkers were obtained.Furtherly,nine targets of ACDP active components were revealed,and they were significantly enriched in PI3 K/AKT and cell cycle signaling pathways.The affinity between these targets and their corresponding active ingredients was predicted by molecular docking.Finally,in vivo and in vitro experiments showed that ACDPs could reduce the activity of PI3 K/AKT signaling pathway and downregulate the expression of cell cycle-related proteins,contributing to the decreased growth of liver cancer.Altogether,PI3 K/AKT-cell cycle appears as the significant central node in anti-liver cancer of A.Cinnamomea.

关键词： Antrodia cinnamomea UPLC-Q-TOF/MS Anti-hepatocellular carcinoma Network pharmacology PI3K/AKT cell cycle

Expression dynamics of periodic transcripts during cancer cell cycle progression and their correlation with anticancer drug sensitivity

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军事医学研究:英文版 2023年第4期10卷 444-460页

作者： Chun‑Xiao Li Jin‑Song Wang Wen‑Na Wang Dong‑Kui Xu Yan‑Tong Zhou Fang‑Zhou Sun Yi‑Qun Li Feng‑Zhu Guo Jia‑Lu Ma Xue‑Yan Zhang Meng‑Jiao Chang Bing‑He Xu Fei Ma Hai‑Li Qian State Key Laboratory of Molecular Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of Medical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of VIP National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China

Background:The cell cycle is at the center of cellular activities and is orchestrated by complex regulatory mechanisms,among which transcriptional regulation is one of the most important components.Alternative splicing dramatically expands the regulatory network by producing transcript isoforms of genes to exquisitely control the cell cycle.However,the patterns of transcript isoform expression in the cell cycle are unclear.Therapies targeting cell cycle checkpoints are commonly used as anticancer therapies,but none of them have been designed or evaluated at the alternative splicing transcript level.The utility of these transcripts as markers of cell cycle-related drug sensitivity is still unknown,and studies on the expression patterns of cell cycle-targeting drug-related transcripts are also rare.Methods:To explore alternative splicing patterns during cell cycle progression,we performed sequential transcriptomic assays following cell cycle synchronization in colon cancer HCT116 and breast cancer MDA-MB-231 cell lines,using flow cytometry and reference cell cycle transcripts to confirm the cell cycle phases of samples,and we developed a new algorithm to describe the periodic patterns of transcripts fluctuating during the cell cycle.Genomics of Drug Sensitivity in Cancer(GDSC)drug sensitivity datasets and Cancer cell Line Encyclopedia(CCLE)transcript datasets were used to assess the correlation of genes and their transcript isoforms with drug sensitivity.We identified transcripts associated with typical drugs targeting cell cycle by determining correlation coefficients.Cytotoxicity assays were used to confirm the effect of ENST00000257904 against cyclin dependent kinase 4/6(CDK4/6)inhibitors.Finally,alternative splicing transcripts associated with mitotic(M)phase arrest were analyzed using an RNA synthesis inhibition assay and transcriptome analysis.Results:We established high-resolution transcriptome datasets of synchronized cell cycle samples from colon cancer HCT116 and breast cancer MDA-MB-231 cells.The results

关键词： cell cycle Alternative splicing Transcriptome Drug resistance Cyclin dependent kinase 4/6 inhibitor,Dolichyl-phosphate mannosyltransferase polypeptide 2

Discovery of small molecule degraders for modulating cell cycle

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Frontiers of Medicine 2023年第5期17卷 823-854页

作者： Liguo Wang Zhouli Yang Guangchen Li Yongbo Liu Chao Ai Yu Rao MOE Key Laboratory of Protein Sciences School of Pharmaceutical SciencesMOE Key Laboratory of Bioorganic Phosphorus Chemistry&Chemical BiologyTsinghua UniversityBeijing100084China Beijing Tsinghua Changgung Hospital School of Clinical MedicineTsinghua UniversityBeijing102218China

The cell cycle is a complex process that involves DNA replication,protein expression,and cell division.Dysregulation of the cell cycle is associated with various diseases.Cyclin-dependent kinases(CDKs)and their corresponding cyclins are major proteins that regulate the cell cycle.In contrast to inhibition,a new approach called proteolysis-targeting chimeras(PROTACs)and molecular glues can eliminate both enzymatic and scaffold functions of CDKs and cyclins,achieving targeted degradation.The field of PROTACs and molecular glues has developed rapidly in recent years.In this article,we aim to summarize the latest developments of CDKs and cyclin protein degraders.The selectivity,application,validation and the current state of each CDK degrader will be overviewed.Additionally,possible methods are discussed for the development of degraders for CDK members that still lack them.Overall,this article provides a comprehensive summary of the latest advancements in CDK and cyclin protein degraders,which will be helpful for researchers working on this topic.

关键词： PROTAC molecular glue degrader cell cycle CDK cyclin

E2F4 regulates the cell cycle and DNA replication in the silkworm,Bombyx mori

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Insect Science 2022年第4期29卷 1006-1016页

作者： Peng Chen Ling Wang Yan-Bi Long Guang-Yan Liang Xiu Yang Zhan-Qi Dong Xia Jiang Yan Zhu Min-Hui Pan Cheng Lu State Key Laboratory of Silkworm Genome Biology Southwest UniversityChongqingChina Key Laboratory of Sericultural Biology and Genetic Breeding Ministry of Agriculture and Rural AffairsSouthwest UniversityChongqingChina

The E2F family of transcription factors is crucial for cell cycle progression and cell fate decisions.Although E2Fs have been widely studied in mammals,there have been few studies performed in insects.Here,we determined the function of E2F4 in the silkworm,Bombyx mori.We demonstrate that E2F proteins are highly conserved among species from lower animals to higher mammals.Overexpression of the BmE2F4 gene led to cell cycle arrest in the G1 phase,whereas interfering with the BmE2F4 mRNA led to accumulation of cells in the S phase.These results indicate that BmE2F4 is important in cell cycle regulation.We also demonstrate that the BmE2F4 gene is involved in DNA replication of BmN-SWU1 cells and DNA synthesis in the silk gland.Furthermore,we identified a protein called Bm14-3-3ζthat can interact with BmE2F4 and allow it to localize in the nucleus.Overexpression of the Bm14-3-3ζgene led to cell cycle arrest in the G1 phase,while knocking down the gene increased the proportion of cells in S phase.These findings provide important insights into the function of E2F transcription factors and increase our understanding of their involvement in cell cycle regulation.

关键词： Bm14-3-35 Bombyx mori cell cycle E2F transcription factors E2F4 insect

Deficiency of two-pore segment channel 2 contributes to systemic lupus erythematosus via regulation of apoptosis and cell cycle

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Chinese Medical Journal 2022年第4期135卷 447-455页

作者： Keke Li Jingkai Xu Ke Xue Ruixing Yu Chengxu Li Wenmin Fei Xiaoli Ning Yang Han Ziyi Wang Jun Shu Yong Cui Department of Dermatology China-Japan Friendship HospitalBeijing 100029China Graduate School of Peking Union Medical College Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Institute of Clinical Medical Science China-Japan Friendship HospitalBeijing 100029China

Background:Systemic lupus erythematosus(SLE)is a complex autoimmune disease,and the mechanism of SLE is yet to be fully elucidated.The aim of this study was to explore the role of two-pore segment channel 2(TPCN2)in SLE pathogenesis.Methods:Quantitative reverse transcription polymerase chain reaction(qRT-PCR)was used to detect the expression ofTPCN2 in SLE.We performed a loss-of-function assay by lentiviral construct in Jurkat and THP-1 cell.Knockdown ofTPCN2 were confirmed at the RNA level by qRT-PCR and protein level by Western blotting.cell Count Kit-8 and flow cytometry were used to analyze the cell proliferation,apoptosis,and cell cycle ofTPCN2-deficient cells.In addition,gene expression profile ofTPCN2-deficient cells was analyzed by RNA sequencing(RNA-seq).Results:TPCN2 knockdown with short hairpin RNA(shRNA)-mediated lentiviruses inhibited cell proliferation,and induced apoptosis and cell-cycle arrest of G2/M phase in both Jurkat and THP-1 cells.We analyzed the transcriptome of knockdown-TPCN2-Jurkat cells,and screened the differential genes,which were enriched for the G2/M checkpoint,complement,and interleukin-6-Janus kinase-signal transducer and activator of transcription pathways,as well as changes in levels of forkhead box O,phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin,and T cell receptor pathways;moreover,TPCN2 significantly influenced cellular processes and biological regulation.Conclusion:TPCN2 might be a potential protective factor against SLE.

关键词： TPCN2 Systemic lupus erythematosus RNA sequencing analysis Apoptosis cell cycle

Cdk5 and aberrant cell cycle activation at the core of neurodegeneration

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Neural Regeneration Research 2023年第6期18卷 1186-1190页

作者： Raquel Requejo-Aguilar Department of Biochemistry and Molecular Biology University of CórdobaCórdobaSpain Maimónides Biomedical Research Institute of Córdoba(IMIBIC) 14071 CórdobaSpain

Neurodegenerative diseases are caused by the progressive loss of specific neurons.The exact mechanisms of action of these diseases are unknown,and many studies have focused on pathways related to abnormal accumulation and processing of proteins,mitochondrial dysfunction,and oxidative stress leading to apoptotic death.However,a growing body of evidence indicates that aberrant cell cycle re-entry plays a major role in the pathogenesis of neurodegeneration.The activation of the cell cycle in mature neurons could be promoted by several signaling mechanisms,including c-Jun N-terminal kinases,p38 mitogen-activated protein kinases,and mitogen-activated protein kinase/extracellular signal-regulated kinase cascades;post-translational modifications such as Tau-phosphorylation;and DNA damage response.In all these events,implicated Cdk5,a proline-directed serine/threonine protein kinase,seems to be responsible for several cellular processes in neurons including axon growth,neurotransmission,synaptic plasticity,neuronal migration,and maintenance of neuronal survival.However,under pathological conditions,Cdk5 dysregulation may lead to cell cycle re-entry in post-mitotic neurons.Thus,Cdk5 hyperactivation,by its physiologic activator p25,hyper-phosphorylates downstream substrates related to neurodegenerative diseases.This review summarizes factors such as oxidative stress,DNA damage response,signaling pathway disturbance,and Ubiquitin proteasome malfunction contributing to cell cycle re-entry in post-mitotic neurons.It also describes how all these factors are linked to a greater or lesser extent with Cdk5.Thus,it offers a global vision of the function of cell cycle-related proteins in mature neurons with a focus on Cdk5 and how this protein contributes to the development of Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis,and Huntington’s disease by cell cycle activation.

关键词： Alzheimer´s disease amyotrophic lateral sclerosis apoptosis Cdk5 cell cycle Huntington´s disease neurodegeneration neuron oxidative stress Parkinson´s disease signaling Tau phosphorylation

Anoctamin 5 regulates the cell cycle and affects prognosis in gastric cancer

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World Journal of Gastroenterology 2022年第32期28卷 4649-4667页

作者： Tomoyuki Fukami Atsushi Shiozaki Toshiyuki Kosuga Michihiro Kudou Hiroki Shimizu Takuma Ohashi Tomohiro Arita Hirotaka Konishi Shuhei Komatsu Takeshi Kubota Hitoshi Fujiwara Kazuma Okamoto Mitsuo Kishimoto Yukiko Morinaga Eiichi Konishi Eigo Otsuji Division of Digestive Surgery Department of SurgeryKyoto Prefectural University of MedicineKyoto 602-8566Japan Department of Pathology Kyoto City HospitalKyoto 604-8845Japan Department of Pathology Kyoto Prefectural University of MedicineKyoto 602-8566Japan

BACKGROUND Anoctamin 5(ANO5)/transmembrane protein 16E belongs to the ANO/transmembrane protein 16 anion channel family.ANOs comprise a family of plasma membrane proteins that mediate ion transport and phospholipid scrambling and regulate other membrane proteins in numerous cell types.Previous studies have elucidated the roles and mechanisms of ANO5 activation in various cancer types.However,it remains unclear whether ANO5 acts as a plasma membrane chloride channel,and its expression and functions in gastric cancer(GC)have not been investigated.AIM To examine the role of ANO5 in the regulation of tumor progression and clinicopathological significance of its expression in GC.METHODS Knockdown experiments using ANO5 small interfering RNA were conducted in human GC cell lines,and changes in cell proliferation,cell cycle progression,apoptosis,and cellular movement were assessed.The gene expression profiles of GC cells were investigated following ANO5 silencing by microarray analysis.Immunohistochemical staining of ANO5 was performed on 195 primary tumor samples obtained from patients with GC who underwent curative gastrectomy between 2011 and 2013 at our department.RESULTS Reverse transcription-quantitative polymerase chain reaction(PCR)and western blotting demonstrated high ANO5 mRNA and protein expression,respectively,in NUGC4 and MKN45 cells.In these cells,ANO5 silencing inhibited cell proliferation and induced apoptosis.In addition,the knockdown of ANO5 inhibited G1-S phase progression,invasion,and migration.The results of the microarray analysis revealed changes in the expression levels of several cyclin-associated genes,such as CDKN1A,CDK2/4/6,CCNE2,and E2F1,in ANO5-depleted NUGC4 cells.The expression of these genes was verified using reverse transcription-quantitative PCR.Immunohistochemical staining revealed that high ANO5 expression levels were associated with a poor prognosis.Multivariate analysis identified high ANO5 expression as an independent prognostic factor for 5-year survival in patients with GC(P=0

关键词： Anoctamin 5 Gastric cancer cell cycle G1/S checkpoint cell proliferation