检索结果-南通市图书馆

Tra2βEnhances Cell Proliferation by Inducing the Expression of Transcription Factor SP1 in Cervical cancer

在线全文

学校读者我要写书评

暂无评论

Biomedical and Environmental Sciences 2023年第2期36卷 146-159页

作者： LI Mo Juan XIONG Dan WANG Shuai HUANG Hao Department of The Sixth Affiliated Hospital School of MedicineSouth China University of Technology(Nanhai District People’s Hospital of Foshan)Foshan 528200GuangdongChina Shunde Hospital Southern Medical University(The First People’s Hospital of Shunde)Foshan 528308GuangdongChina

Objective In this study,the role and potential mechanism of transformer 2β(Tra2β)in Cervical cancer were explored.Methods The transcriptional data of Tra2βin patients with Cervical cancer from Gene Expression Profiling Interactive Analysis(GEPIA)and cBioPortal databases were investigated.The functions of Tra2βwere evaluated by using Western blot,MTT,colony formation,Transwell assays,and nude mouse tumor formation experiments.Target genes regulated by Tra2βwere studied by RNA-seq.Subsequently,representative genes were selected for RT-qPCR,confocal immunofluorescence,Western blot,and rescue experiments to verify their regulatory relationship.Results The dysregulation of Tra2βin Cervical cancer samples was observed.Tra2βoverexpression in Siha and Hela cells enhanced cell viability and proliferation,whereas Tra2βknockdown showed the opposite effect.Alteration of Tra2βexpression did not affect cell migration and invasion.Furthermore,tumor xenograft models verified that Tra2βpromoted Cervical cancer growth.Mechanically,Tra2βpositively regulated the mRNA and protein level of SP1,which was critical for the proliferative capability of Tra2β.Conclusion This study demonstrated the important role of the Tra2β/SP1 axis in the progression of Cervical cancer in vitro and in vivo,which provides a comprehensive understanding of the pathogenesis of Cervical cancer.

关键词： Tra2β Cervical cancer Proliferation SP1 Molecular targeted therapy

Casticin Attenuates Stemness in Cervical cancer Stem-Like Cells by Regulating Activity and Expression of DNMT1

在线全文

学校读者我要写书评

暂无评论

Chinese Journal of Integrative Medicine 2023年第3期29卷 224-232页

作者： WANG Xue-li CAO Xiao-zheng WANG Dao-yuan QIU Ye-bei DENG Kai-yu CAO Jian-guo LIN Shao-qiang XU Yong REN Kai-qun Medical College Hunan University of MedicineHuaihuaHunan Province(418000)China Clinical Department of Guangdong Metabolic Disease Research Centre of Integrated Chinese and Western Medicine the First Affiliated Hospital of Guangdong Pharmaceutical UniversityGuangzhou(510062)China Institute of Chemical Biology Guangzhou Institutes of Biomedicine and HealthChinese Academy of SciencesGuangzhou(510530)China The Key Laboratory of Model Animals and Stem Cell Biology in Hunan Province Medical CollegeHunan Normal UniversityChangsha(410013)China The Key Laboratory of Study and Discover of Small Targeted Molecules of Hunan Province Medical CollegeHunan Normal UniversityChangsha(410013)China

Objective:To explore whether casticin(CAS)suppresses stemness in cancer stem-like cells(CSLCs)obtained from human Cervical cancer(CCSLCs)and the underlying mechanism.Methods:Spheres from He La and Ca Ski cells were used as CCSLCs.DNA methyltransferase 1(DNMT1)activity and m RNA levels,self-renewal capability(Nanog and Sox2),and cancer stem cell markers(CD133 and CD44)were detected by a colorimetric DNMT activity/inhibition assay kit,quantitative real-time reverse transcription-polymerase chain reaction,sphere and colony formation assays,and immunoblot,respectively.Knockdown and overexpression of DNMT1 by transfection with sh RNA and c DNA,respectively,were performed to explore the mechanism for action of CAS(0,10,30,and 100 nmol/L).Results:DNMT1 activity was increased in CCSLCs compared with He La and Ca Ski cells(PCervical cancer.

关键词： Cervical cancer cancer stem cell casticin DNA methyltransferase 1 therapeutic action

Cervical cancer:a tale from HPV infection to PARP inhibitors

在线全文

学校读者我要写书评

暂无评论

Genes & Diseases 2023年第4期10卷 1445-1456页

作者： Minakshi Mann Vikram Pratap Singh Lalit Kumar Department of Medical Oncology Dr.B.R.A.Institute Rotary Cancer HospitalAll India Institute of Medical SciencesNew Delhi 110029India Department of Oncoanaesthesia and Palliative Medicine Dr.B.R.A.Institute Rotary Cancer HospitalAll India Institute of Medical SciencesNew Delhi 110029India Epigenetics Section Mouse Cancer Genetics ProgramCenter for Cancer ResearchNational Cancer InstituteFrederickMD 21702USA

Globally,Cervical cancer(CxCa)ranks 4th common cancer among females and led to 569,847 incidences and 311,365 deaths in 2018.80%of CxCa cases occur due to persistent infection with a high-risk subtype of human papillomavirus(HPV-16 and 18).Smoking,high par-ity,and co-infection with type 2 herpes simplex or HIV are other known risk factors for CxCa.Major histological subtypes are squamous(70%)and adenocarcinoma(25%).Presently,concur-rent radiation plus cisplatin(CDDP)-based chemotherapy is the standard treatment for CxCa patients.However,CDDP resistance and toxic side effects limit its efficacy,leading to a poorer response rate and an expected overall survival ranging from 10 to 17.5 months.Reduced drug uptake,increased DNA damage repair,increased CDDP inactivation,and overexpressed Bcl-2 or caspase inhibition,are primarily accountable mechanisms for CDDP resistance and improving CDDP’s efficacy remains the major challenge.Poly(ADP-ribosyl)polymerase-1,an effective mediator of nucleotide excision repair pathway,is involved in DNA repair as well as maintaining genomic stability and is significantly expressed in malignant lymphomas,hepa-tocellular-,cervical-and colorectal carcinoma,which has been approved effective in mainte-nance therapy and may serve as an effective target to enhance CDDP sensitivity in CxCa.Here,we summarize the etiology and epidemiology of and treatment for CxCa,the mechanism responsible for chemotherapy resistance,PARP inhibitor as a possible therapy for CxCa,and other possible chemotherapeutic options for CxCa treatment.

关键词： Cervical cancer Chemotherapy Cisplatin Disease etiology and histology PARP inhibitors Resistance

The suppression of Cervical cancer ferroptosis by macrophages:The attenuation of ALOX15 in cancer cells by macrophages-derived exosomes

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

药学学报:英文版 2023年第6期13卷 2645-2662页

作者： Yanlin Luo Yibing Chen Huan Jin Benxin Hou Hongsheng Li Xiang Li Lingfeng Liu Yuan Zhou Yonghua Li Yong Sang Song Quentin Liu Zhengzhi Zou Department of Gynecologic Oncology the Affiliated Cancer Hospital of Zhengzhou University&Henan Cancer HospitalZhengzhou 450001China MOE Key Laboratory of Laser Life Science&Institute of Laser Life Science Guangdong Provincial Key Laboratory of Laser Life ScienceCollege of BiophotonicsSouth China Normal UniversityGuangzhou 510631China Institute of Clinical Pharmacology School of Basic Medical ScienceAcademy of Medical ScienceZhengzhou UniversityZhengzhou 450001China Genetic and Prenatal Diagnosis Center Department of Gynecology and ObstetricsFirst Affiliated HospitalZhengzhou UniversityZhengzhou 450001China Department of General Surgery the Third People's Hospital of Hainan ProvinceSanya 572000China Department of Breast Surgery Affiliated Cancer Hospital&Institute of Guangzhou Medical UniversityGuangzhou 510095China Department of Pathophysiology School of Basic Medical SciencesZhengzhou UniversityZhengzhou 450001China Department of Obstetrics and Gynecology Cancer Research InstituteCollege of MedicineSeoul National UniversitySeoul 03080South Korea State Key Laboratory of Oncology in South China Cancer CenterSun Yat-sen UniversityGuangzhou 510631China Guangzhou Key Laboratory of Spectral Analysis and Functional Probes College of BiophotonicsSouth China Normal UniversityGuangzhou 510631China

Induction of cancer cell ferroptosis has been proposed as a potential treatment in several cancer types.Tumor-associated macrophages(TAMs)play a key role in promoting tumor malignant progression and therapy resistance.However,the roles and mechanisms of TAMs in regulating tumor ferroptosis is still unexplored and remains enigmatic.This study shows ferroptosis inducers has shown therapeutic outcomes in Cervical cancer in vitro and in vivo.TAMs have been found to suppress Cervical cancer cells ferroptosis.Mechanistically,macrophage-derived miRNA-660-5p packaged into exosomes are transported into cancer cells.In cancer cells,miRNA-660-5p attenuates ALOX15 expression to inhibit ferroptosis.Moreover,the upregulation of miRNA-660-5p in macrophages depends on autocrine IL4/IL13-activated STAT6 pathway.Importantly,in clinical Cervical cancer cases,ALOX15 is negatively associated with macrophages infiltration,which also raises the possibility that macrophages reduce ALOX15 levels in Cervical cancer.Moreover,both univariate and multivariate Cox analyses show ALOX15 expression is independent prognostic factor and positively associated with good prognosis in Cervical cancer.Altogether,this study reveals the potential utility of targeting TAMs in ferroptosis-based treatment and ALOX15 as prognosis indicators for Cervical cancer.

关键词： Cervical cancer Tumor-associated macrophage ALOX15 Ferroptosis Exosome miRNA-660-5p Macrophages infiltration STAT6

Adjuvant chemotherapy versus adjuvant concurrent chemoradiotherapy after radical surgery for early-stage Cervical cancer:a randomized,non-inferiority,multicenter trial

在线全文

学校读者我要写书评

暂无评论

Frontiers of Medicine 2023年第1期17卷 93-104页

作者： Danhui Weng Huihua Xiong Changkun Zhu Xiaoyun Wan Yaxia Chen Xinyu Wang Youzhong Zhang Jie Jiang Xi Zhang Qinglei Gao Gang Chen Hui Xing Changyu Wang Kezhen Li Yaheng Chen Yuyan Mao Dongxiao Hu Zimin Pan Qingqin Chen Baoxia Cui Kun Song Cunjian Yi Guangcai Peng Xiaobing Han Ruifang An Liangsheng Fan Wei Wang Tingchuan Xiong Yile Chen Zhenzi Tang Lin Li Xingsheng Yang Xiaodong Cheng Weiguo Lu Hui Wang Beihua Kong Xing Xie Ding Ma Department of Obstetrics and Gynecology Tongji Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Oncology Tongji Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Gynecologic Oncology Women’s HospitalSchool of MedicineZhejiang UniversityHangzhou 310006China Department of Obstetrics and Gynecology Qilu HospitalShandong UniversityJinan 250012China Department of Obstetrics and Gynecology Xiangyang Central HospitalHubei University of Arts and ScienceXiangyang 441021China Department of Obstetrics and Gynecology The First Affiliated Hospital of Yangtze UniversityJingmen 448000China Department of Obstetrics and Gynecology The First Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710061China Department of Obstetrics and Gynecology The First Affiliated Hospital of Guangzhou Medical UniversityGuangzhou 510120China Department of Gynecologic Oncology Affiliated Tumour HospitalXinjiang Medical UniversityUrumqi 830000China Department of Gynecologic Oncology Hunan Province Tumor HospitalChangsha 410013China

We conducted a prospective study to assess the non-inferiority of adjuvant chemotherapy alone versus adjuvant concurrent chemoradiotherapy (CCRT) as an alternative strategy for patients with early-stage (FIGO 2009 stage IB–IIA) Cervical cancer having risk factors after surgery. The condition was assessed in terms of prognosis, adverse effects, and quality of life. This randomized trial involved nine centers across China. Eligible patients were randomized to receive adjuvant chemotherapy or CCRT after surgery. The primary end-point was progression-free survival (PFS). From December 2012 to December 2014, 337 patients were subjected to randomization. Final analysis included 329 patients, including 165 in the adjuvant chemotherapy group and 164 in the adjuvant CCRT group. The median follow-up was 72.1 months. The three-year PFS rates were both 91.9%, and the five-year OS was 90.6% versus 90.0% in adjuvant chemotherapy and CCRT groups, respectively. No significant differences were observed in the PFS or OS between groups. The adjusted HR for PFS was 0.854 (95% confidence interval 0.415–1.757;P = 0.667) favoring adjuvant chemotherapy, excluding the predefined non-inferiority boundary of 1.9. The chemotherapy group showed a tendency toward good quality of life. In comparison with post-operative adjuvant CCRT, adjuvant chemotherapy treatment showed non-inferior efficacy in patients with early-stage Cervical cancer having pathological risk factors. Adjuvant chemotherapy alone is a favorable alternative post-operative treatment.

关键词： chemotherapy Cervical cancer lymph node metastasis concurrent chemoradiotherapy quality of life

Apoptotic and autophagic death union by Thuja occidentalis homeopathic drug in Cervical cancer cells with thujone as the bioactive principle

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Journal of Integrative Medicine 2022年第5期20卷 463-472页

作者： Asmita Pal Sucharita Das Soumalee Basu Rita Kundu Department of Botany University of CalcuttaKolkataWest Bengal 700019India Department of Microbiology University of CalcuttaKolkataWest Bengal 700019India

Objective‘Multi-targeting’drugs can prove fruitful to combat drug-resistance of multifactorial disease—Cervical cancer.This study envisioned to reveal if Thuja homeopathic mother tincture(MT)and its bioactive component could combat human papillomavirus(HPV)-16-infected SiHa Cervical cancer cells since it is globally acclaimed for HPV-mediated warts.Methods Thuja MT was studied for its antiproliferative and antimigratory properties in SiHa cells followed by microscopic determination of reactive oxygen species(ROS)generation by 2’,7’-dichlorodihydrofluorescein diacetate(DCFDA)staining and loss in mitochondrial membrane potential(MMP)by rhodamine(Rh)123 staining.Apoptosis and autophagy inductions were studied by acridine orange(AO)ethidium bromide(EB)staining and immunoblot analyses of marker proteins.The bioactive component of Thuja MT detected by gas chromatography-mass spectrometry was studied for antiproliferative and antimigratory properties along with in silico prediction of its cellular targets by molecular docking and oral drug forming competency.Results Thuja MT showed significant antiproliferative and antimigratory potential in SiHa cells at a 50%inhibitory concentration(IC50)dosage of 17.3μL/mL.An increase in DCFDA fluorescence and loss in Rh123 fluorescence prove that Thuja MT acted through the burst of ROS and loss in MMP respectively.AO/EB-stained cells under the microscope and immunoblot analyses supported Thuja-induced cellular demise via dual pathways—apoptosis and autophagy.Immunoblots showed cleavage of caspase-3 and poly adenosine diphosphate-ribose polymerase-1(PARP-1)along with upregulation of Beclin-1,microtubule-associated protein 1 light chain 3B(LC3B)-II,and p62 proteins.Hence,the apoptotic cascade followed a caspase-3-dependent pathway supported by PARP-1 cleavage,while autophagic death was Beclin-1-dependent and mediated by accumulation of LC3BII and p62 proteins.Thujone,detected as the bioactive principle of Thuja MT showed greater anti-proliferative and anti-migratory potential at an IC

关键词： Thuja Homeopathy Thujone Cervical cancer Apoptosis-autophagy crosstalk

Histone deacetylase inhibitors inhibit Cervical cancer growth through Parkin acetylationmediated mitophagy

在线全文

学校读者我要写书评

暂无评论

Acta Pharmaceutica Sinica B 2022年第2期12卷 838-852页

作者： Xin Sun Yuhan Shu Guiqin Ye Caixia Wu Mengting Xu Ruilan Gao Dongsheng Huang Jianbin Zhang Department of Oncology Cancer Center of Zhejiang Provincial People’s HospitalAffiliated People’s HospitalHangzhou Medical CollegeHangzhou 310014China Clinical Research Institute Zhejiang Provincial People’s HospitalAffiliated People’s HospitalHangzhou Medical CollegeHangzhou 310014China Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province Hangzhou Medical CollegeHangzhou 310014China College of Biomedical Engineering&Instrument Science Zhejiang UniversityHangzhou 310028China Department of Hematology the First Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310006China

Parkin,an E3 ubiquitin ligase,plays a role in maintaining mitochondrial homeostasis through targeting damaged mitochondria for mitophagy.Accumulating evidence suggests that the acetylation modification of the key mitophagy machinery influences mitophagy level,but the underlying mechanism is poorly understood.Here,our study demonstrated that inhibition of histone deacetylase(HDAC)by treatment of HDACis activates mitophagy through mediating Parkin acetylation,leading to inhibition of Cervical cancer cell proliferation.Bioinformatics analysis shows that Parkin expression is inversely correlated with HDAC2 expression in human Cervical cancer,indicating the low acetylation level of Parkin.Using mass spectrometry,Parkin is identified to interact with two upstream molecules,acetylase acetyl-Co A acetyltransferase 1(ACAT1)and deacetylase HDAC2.Under treatment of suberoylanilide hydroxamic acid(SAHA),Parkin is acetylated at lysine residues 129,220 and 349,located in different domains of Parkin protein.In in vitro experiments,combined mutation of Parkin largely attenuate the interaction of Parkin with PTEN induced putative kinase 1(PINK1)and the function of Parkin in mitophagy induction and tumor suppression.In tumor xenografts,the expression of mutant Parkin impairs the tumor suppressive effect of Parkin and decreases the anticancer activity of SAHA.Our results reveal an acetylation-dependent regulatory mechanism governing Parkin in mitophagy and cervical carcinogenesis,which offers a new mitophagy modulation strategy for cancer therapy.

关键词： Parkin Mitophagy ACAT1 HDAC2 Acetylation Ubiquitination Tumor suppression Cervical cancer

N^(6)-methyladenosine modification of CENPK mRNA by ZC3H13 promotes Cervical cancer stemness and chemoresistance

在线全文

学校读者我要写书评

暂无评论

Military Medical Research 2022年第5期9卷 576-591页

作者： Xian Lin Feng Wang Jian Chen Jing Liu Yi-Bin Lin Li Li Chuan-Ben Chen Qin Xu Departments of Gynecology Fujian Cancer Hospital and Fujian Medical University Cancer HospitalFujian Medical UniversityFuzhou 350014China Department of Radiation Oncology Fujian Cancer Hospital and Fujian Medical University Cancer HospitalFujian Medical UniversityFuzhou 350014China Shenzhen Key Laboratory of Immunity and Inflammatory Diseases Peking University Shenzhen HospitalShenzhen Peking University?the Hong Kong University of Science and Technology Medical CenterShenzhen 518036GuangdongChina Outpatient Department Fujian Hospital of People's Armed PoliceFujian Medical UniversityFuzhou 350014China

Background:Stemness and chemoresistance contribute to Cervical cancer recurrence and metastasis.In the current study,we determined the relevant players and role of N^(6)-methyladenine(m^(6)A)RNA methylation in Cervical cancer progression.Methods:The roles of m^(6)A RNA methylation and centromere protein K(CENPK)in Cervical cancer were analyzed using bioinformatics analysis.Methylated RNA immunoprecipitation was adopted to detect m^(6)A modification of CENPK mRNA.Human Cervical cancer clinical samples,cell lines,and xenografts were used for analyzing gene expression and function.Immunofluorescence staining and the tumorsphere formation,clonogenic,MTT,and EdU assays were performed to determine cell stemness,chemoresistance,migration,invasion,and proliferation in HeLa and SiHa cells,respectively.Western blot analysis,co-immunoprecipitation,chromatin immunoprecipitation,and luciferase reporter,cycloheximide chase,and cell fractionation assays were performed to elucidate the underlying mechanism.Results:Bioinformatics analysis of public cancer datasets revealed firm links between m^(6)A modification patterns and Cervical cancer prognosis,especially through ZC3H13-mediated m^(6)A modification of CENPK mRNA.CENPK expression was elevated in Cervical cancer,associated with cancer recurrence,and independently predicts poor patient prognosis[hazard ratio=1.413,95%confidence interval=1.078−1.853,P=0.012].Silencing of CENPK prolonged the overall survival time of Cervical cancer-bearing mice and improved the response of Cervical cancer tumors to chemotherapy in vivo(P<0.001).We also showed that CENPK was directly bound to SOX6 and disrupted the interactions of CENPK withβ-catenin,which promotedβ-catenin expression and nuclear translocation,facilitated p53 ubiquitination,and led to activation of Wnt/β-catenin signaling,but suppression of the p53 pathway.This dysregulation ultimately enhanced the tumorigenic pathways required for cell stemness,DNA damage repair pathways necessary for cisplatin/carboplatin resistance,epithelial-m

关键词： N^(6)-methyladenosine Centromere protein K Cervical cancer Stemness Chemoresistance

Bioinformatic and Experimental Analyses Reveal That KIF4A Is a Biomarker of Therapeutic Sensitivity and Predicts Prognosis in Cervical cancer Patients

在线全文

学校读者我要写书评

暂无评论

Current Medical Science 2022年第6期42卷 1273-1284页

作者： Jie WU Lan LI Hao ZHONG Hao-han ZHANG Jing LI Hui-bo ZHANG Ya-qi ZHAO Bin XU Qi-bin SONG cancer Center Renmin Hospital of Wuhan UniversityWuhan430030China Department of Bioinformatics Wissenschaftszentrum WeihenstephanTechnical University of MunichFreising85354Germany

Objective This study aims to investigate the expression,prognostic value,and function of kinesin superfamily 4A(KIF4A)in Cervical cancer.Methods Cervical cancer cell lines(Hela and SiHa)and TCGA data were used for experimental and bioinformatic analyses.Overall survival(OS)and progression free survival(PFS)were compared between patients with high or low KIF4A expression.Copy number variation(CNV)and somatic mutations of patients were visualized and GISTIC 2.0 was used to identify significantly altered sites.The function of KIF4A was also explored based on transcriptome analysis and validated by experimental methods.Chemotherapeutic and immunotherapeutic benefits were inferred using multiple reference databases and algorithms.Results Patients with high KIF4A expression had better OS and PFS.KIF4A could inhibit proliferation and migration and induce G1 arrest of Cervical cancer cells.Higher CNV load was observed in patients with low KIF4A expression,while the group with low KIF4A expression displayed more significantly altered sites.A total of 13 genes were found to mutate more in the low KIF4A expression group,including NOTCH1 and PUM1.The analysis revealed that low KIF4A expression may indicate an immune escape phenotype,and patients in this group may benefit more from immunotherapy.With respect to chemotherapy,cisplatin and gemcitabine may respond better in patients with high KIF4A expression,while 5-fluorouracil etc.may be responded better in patients with low KIF4A expression Conclusion KIF4A is a tumor suppressor gene in Cervical cancer,and it can be used as a prognostic and therapeutic biomarker in Cervical cancer.

关键词： kinesin superfamily 4A Cervical cancer prognosis chemotherapy immunotherapy