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Baicalin Antagonizes Prostate cancer stemness via Inhibiting Notch1/NF-κB Signaling Pathway

中国结合医学杂志:英文版 2023年第10期29卷 914-923页

作者： WU Ming-hui WU Kun ZHU Yuan-bing LI Da-chuan YANG Huan ZENG Hong Department of Urology Hubei University of Traditional Chinese MedicineWuhan430065China Department of Urology Chongqing Jiangjin District Hospital of Chinese MedicineChongqing402260China

Objective To investigate the molecular mechanisms underlying the effect of baicalin on prostate cancer(PCa)progression both in vivo and in vitro.Methods The in situ PCa stem cells(PCSCs)-injected xenograft tumor models were established in BALB/c nude mice.Tumor volume and weight were respectively checked after baicalin(100 mg/kg)treatment.Hematoxylin-eosin(HE)staining was used to observe the growth arrest and cell necrosis.mRNA expression levels of acetaldehyde dehydrogenase 1(ALDH1),CD44,CD133 and Notch1 were determined by reverse transcription-polymerase chain reaction.Protein expression levels of ALDH1,CD44,CD133,Notch1,nuclear factorκB(NF-κB)P65 and NF-κB p-P65 were detected by Western blot.Expression and subcellular location of ALDH1,CD44,CD133,Notch1 and NF-κB p65 were detected by immunofluorescence analysis.In vitro,cell cycle distribution and cell apoptosis of PC3 PCSCs was assessed by flow cytometry after baicalin(125µmol/L)treatment.The migration and invasion abilities of PCSCs were assessed using Transwell assays.Transmission electron microscopy scanning was utilized to observe the structure and autophagosome formation of baicalin-treated PCSCs.In addition,PCSCs were infected with lentiviruses expressing human Notch1.Results Compared with the control group,the tumor volume and weight were notably reduced in mice treated with 100 mg/kg baicalin(P<0.05 or P<0.01).Histopathological analysis showed that baicalin treatment significantly inhibited cell proliferation and promoted cell apoptosis.Furthermore,baicalin treatment reduced mRNA and protein expression levels of CD44,CD133,ALDH1,and Notch1 as well as the protein expression of NF-κB p-P65 in the xenograft tumor(P<0.01).In vitro,the cell proliferation of PCSCs was significantly attenuated after treatment with 125µmol/L baicalin for 72 h(P<0.01).The cell migration and invasion rates were decreased following treatment with baicalin for 48 and 72 h(P<0.01).Baicalin notably induced cell apoptosis and seriously damaged the structure of PCSCs.The mRNA and pro

关键词： baicalin prostate cancer cancer stemness Notch1/nuclear factorκB signaling

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Physical exercise suppresses hepatocellular carcinoma progression by alleviating hypoxia and attenuating cancer stemness through the Akt/GSK-3β/β-catenin pathway

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Journal of Integrative Medicine 2023年第2期21卷 184-193页

作者： Chu-lan Xiao Zhi-peng Zhong Can Lü Bing-jie Guo Jiao-jiao Chen Tong Zhao Zi-fei Yin Bai Li Department of Rehabilitation Changhai HospitalNaval Medical UniversityShanghai 200433China Department of Traditional Chinese Medicine The 920th Hospital of Joint Logistics Support ForceKunming 650000Yunnan ProvinceChina Second Team Graduate SchoolNaval Medical UniversityShanghai 200433China College of Integrated Traditional Chinese and Western Medicine Nanjing University of Traditional Chinese MedicineNanjing 210023Jiangsu ProvinceChina Department of Military Traditional Chinese Medicine Faculty of Traditional Chinese MedicineNaval Medical UniversityShanghai 200433China

Objective:Physical exercise,a common non-drug intervention,is an important strategy in cancer treatment,including hepatocellular carcinoma(HCC).However,the mechanism remains largely unknown.Due to the importance of hypoxia and cancer stemness in the development of HCC,the present study investigated whether the anti-HCC effect of physical exercise is related to its suppression on hypoxia and cancer stemness.Methods:A physical exercise intervention of swimming(30 min/d,5 d/week,for 4 weeks)was administered to BALB/c nude mice bearing subcutaneous human HCC tumor.The anti-HCC effect of swimming was assessed in vivo by tumor weight monitoring,hematoxylin and eosin(HE)staining,and immunohistochemistry(IHC)detection of proliferating cell nuclear antigen(PCNA)and Ki67.The expression of stemness transcription factors,including Nanog homeobox(NANOG),octamer-binding transcription factor 4(OCT-4),v-Myc avian myelocytomatosis viral oncogene homolog(C-MYC)and hypoxia-inducible factor-1a(HIF-1a),was detected using real-time reverse transcription polymerase chain reaction.A hypoxia probe was used to explore the intratumoral hypoxia status.Western blot was used to detect the expression of HIF-1a and proteins related to protein kinase B(Akt)/glycogen synthase kinase-3β(GSK-3β)/β-catenin signaling pathway.The IHC analysis of platelet endothelial cell adhesion molecule-1(CD31),and the immunofluorescence co-location of CD31 and desmin were used to analyze tumor blood perfusion.SMMC-7721 cells were treated with nude mice serum.The inhibition effect on cancer stemness in vitro was detected using suspension sphere experiments and the expression of stemness transcription factors.The hypoxia status was inferred by measuring the protein and mRNA levels of HIF-1a.Further,the expression of proteins related to Akt/GSK-3β/β-catenin signaling pathway was detected.Results:Swimming significantly reduced the body weight and tumor weight in nude mice bearing HCC tumor.HE staining and IHC results showed a lower necrotic area ratio as well as fewer

关键词： Physical exercise Swimming Hepatocellular carcinoma Liver cancer Blood perfusion Hypoxia cancer stemness Akt/GSK-3β/β-catenin

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PLEK2 promotes cancer stemness and tumorigenesis of head and neck squamous cell carcinoma via the c-Myc-mediated positive feedback loop

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cancer Communications 2022年第10期42卷 987-1007页

作者： Xinyuan Zhao Dalong Shu Wenjuan Sun Shanshan Si Wei Ran Bing Guo Li Cui Department of Endodontics Stomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280P.R.China Department of Oral and Maxillofacial Surgery The First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Stomatology The Third Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510630P.R.China Department of Oral Emergency Stomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280P.R.China Department of Dentistry The First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Oral and Maxillofacial Surgery Stomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280P.R.China Division of Oral Biology and Medicine School of DentistryUniversity of CaliforniaLos AngelesLos AngelesCalifornia 90095United States

Background:Head and neck squamous cell carcinoma(HNSCC)is one of the most frequent malignancies worldwide and is characterized by unfavorable prognosis,high lymph node metastasis and early recurrence.However,the molecular events regulating HNSCC tumorigenesis remain poorly understood.Therefore,uncovering the underlying mechanisms is urgently needed to identify novel and promising therapeutic targets for HNSCC.In this study,we aimed to explore the role of pleckstrin-2(PLEK2)in regulating HNSCC tumorigenesis.Methods:The expression pattern of PLEK2 and its clinical significance in HNSCC were determined by analyzing publicly assessable datasets and our own independent HNSCC cohort.In vitro and in vivo experiments,including cell proliferation,colony formation,Matrigel invasion,tumor sphere formation,ALDEFLUOR,Western blotting assays and xenograft mouse models,were used to investigate the role of PLEK2 in regulating the malignant behaviors of HNSCC cells.The underlying molecular mechanisms for the tumor-promoting role of PLEK2 were elucidated using co-immunoprecipitation,cycloheximide chase analysis,ubiquitination assays,chromatin immunoprecipitation-quantitative polymerase chain reaction,luciferase reporter assays and rescue experiments.Results:The expression levels of PLEK2 mRNA and protein were significantly increased in HNSCC tissues,and PLEK2 overexpression was strongly associated with poor overall survival and therapeutic resistance.Additionally,PLEK2 was important for maintaining the proliferation,invasion,epithelial-mesenchymal transition,cancer stemness and tumorigenesis of HNSCC cells and could alter the cellular metabolism of the cancer cells.Mechanistically,PLEK2 interacted with c-Myc and reduced the association of F-box and WD repeat domain containing 7(FBXW7)with c-Myc,thereby avoiding ubiquitination and subsequent proteasome-mediated degradation of c-Myc.Moreover,the c-Myc signaling activated by PLEK2 was important for sustaining the aggressive malignant phenotypes and tumorigenesis of HNSCC cells.c-M

关键词： c-Myc cancer stemness FBXW7 HNSCC PLEK2 positive feedback loop tumorigenesis ubiquitination-mediated degradation

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Jiedu Recipe,a compound Chinese herbal medicine,inhibits cancer stemness in hepatocellular carcinoma via Wnt/β-catenin pathway under hypoxia

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结合医学学报:英文版 2023年第5期21卷 474-486页

作者： Bing-jie Guo Yi Ruan Ya-jing Wang Chu-lan Xiao Zhi-peng Zhong Bin-bin Cheng Juan Du Bai Li Wei Gu Zi-fei Yin School of Traditional Chinese Medicine Naval Medical UniversityShanghai 200433China Department of Gastroenterology Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghai 200433China PLA Naval Medical Center Shanghai 200052China Department of Traditional Chinese Medicine the 920th Hospital of Joint Logistics Support ForceKunming 650000Yunan ProvinceChina Department of Rehabilitation Changhai HospitalNaval Medical UniversityShanghai 200433China

Objective Jiedu Recipe(JR),a Chinese herbal remedy,has been shown to prolong overall survival time and decrease recurrence and metastasis rates in patients with hepatocellular carcinoma(HCC).This work investigated the mechanism of JR in HCC treatment.Methods The chemical constituents of JR were detected using liquid chromatography-mass spectrometry.The potential anti-HCC mechanism of JR was screened using network pharmacology and messenger ribonucleic acid(mRNA)microarray chip assay,followed by experimental validation in human HCC cells(SMMC-7721 and Huh7)in vitro and a nude mouse subcutaneous transplantation model of HCC in vivo.HCC cell characteristics of proliferation,migration and invasion under hypoxic setting were investigated using thiazolyl blue tetrazolium bromide,wound healing and Transwell assays,respectively.Image-i^(TM)Hypoxia Reagent was added to reveal hypoxic conditions.Stem cell sphere formation assay was used to detect the stemness.Epithelial-mesenchymal transition(EMT)markers like E-cadherin,vimentin andα-smooth muscle actin,and pluripotent transcription factors including nanog homeobox,octamer-binding transcription factor 4,and sex-determining region Y box protein 2 were analyzed using Western blotting and real-time polymerase chain reaction.Western blot was performed to ascertain the anti-HCC effect of JR under hypoxia involving the Wnt/β-catenin pathway.Results According to network pharmacology and mRNA microarray chip analysis,JR may potentially act on hypoxia and inhibit the Wnt/β-catenin pathway.In vitro and in vivo experiments showed that JR significantly decreased hypoxia,and suppressed HCC cell features of proliferation,migration and invasion;furthermore,the hypoxia-induced increases in EMT and stemness marker expression in HCC cells were inhibited by JR.Results based on the co-administration of JR and an agonist(LiCl)or inhibitor(IWR-1-endo)verified that JR suppressed HCC cancer stem-like properties under hypoxia by blocking the Wnt/β-catenin pathway.Conclusion JR exerts potent anti-H

关键词： Jiedu Recipe Chinese medicine Hepatocellular carcinoma Hypoxia cancer stemness Wnt/β-cateninpathway

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EMT-associated microRNAs and their roles in cancer stemness and drug resistance

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cancer Communications 2021年第3期41卷 199-217页

作者： Guangtao Pan Yuhan Liu Luorui Shang Fangyuan Zhou Shenglan Yang Department of Traditional Chinese Medicine Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430022P.R.China

Epithelial-to-mesenchymal transition(EMT)is implicated in a wide array of malignant behaviors of cancers,including proliferation,invasion,and metastasis.Most notably,previou studies have indicated that both cancer stem-like properties and drug resistance were associated with EMT.Furthermore,microRNAs(miRNAs)play a pivotal role in the regulation of EMT phenotype,as a result,some miRNAs impact cancer stemness and drug resistance.Therefore,understanding the relationship between EMT-associated miRNAs and cancer stemness/drug resistance is beneficial to both basic research and clinical treatment.In this review,we preliminarily looked into the various roles that the EMT-associated miRNAs play in the stem-like nature of malignant cells.Then,we reviewed the interaction between EMT-associated miRNAs and the drugresistant complex signaling pathways of multiple cancers including lung cancer,gastric cancer,gynecologic cancer,breast cancer,liver cancer,colorectal cancer,pancreatic cancer,esophageal cancer,and nasopharyngeal cancer.We finally discussed the relationship between EMT,cancer stemness,and drug resistance,as well as looked forward to the potential applications of miRNA therapy for malignant tumors.

关键词： cancer epithelial-to-mesenchymal transition microRNA cancer stem cell cancer stemness drug resistance

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Systematic screening reveals synergistic interactions that overcome MAPK inhibitor resistance in cancer cells

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cancer Biology & Medicine 2022年第2期19卷 229-252页

作者： Yu Yu Minzhen Tao Libin Xu Lei Cao Baoyu Le Na An Jilin Dong Yajie Xu Baoxing Yang Wei Li Bing Liu Qiong Wu Yinying Lu Zhen Xie Xiaohua Lian Department of Cell Biology Basic Medical CollegeArmy Medical University(Third Military Medical University)Chongqing 400038China MOE Key Laboratory of Bioinformatics and Bioinformatics Division Center for Synthetic and System BiologyDepartment of AutomationBeijing National Research Center for Information Science and TechnologyTsinghua UniversityBeijing 100084China National cancer Center/National Clinical Research Center for cancer/cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of Thoracic Surgery Peking Union Medical College HospitalChinese Academy of Medical SciencesBeijing 100730China Beijing Syngentech Co. LtdBeijing 102206China School of Life Sciences Tsinghua UniversityBeijing 100084China The Comprehensive Liver cancer Center The 5th Medical Center of PLA General HospitalBeijing 100039China

Objective:Effective adjuvant therapeutic strategies are urgently needed to overcome MAPK inhibitor(MAPKi)resistance,which is one of the most common forms of resistance that has emerged in many types of cancers.Here,we aimed to systematically identify the genetic interactions underlying MAPKi resistance,and to further investigate the mechanisms that produce the genetic interactions that generate synergistic MAPKi resistance.Methods:We conducted a comprehensive pair-wise sgRNA-based high-throughput screening assay to identify synergistic interactions that sensitized cancer cells to MAPKi,and validated 3 genetic combinations through competitive growth,cell viability,and spheroid formation assays.We next conducted Kaplan-Meier survival analysis based on The cancer Genome Atlas database and conducted immunohistochemistry to determine the clinical relevance of these synergistic combinations.We also investigated the MAPKi resistance mechanisms of these validated synergistic combinations by using co-immunoprecipitation,Western blot,qRTPCR,and immunofluorescence assays.Results:We constructed a systematic interaction network of MAPKi resistance and identified 3 novel synergistic combinations that effectively targeted MAPKi resistance(ITGB3+IGF1R,ITGB3+JNK,and HDGF+LGR5).We next analyzed their clinical relevance and the mechanisms by which they sensitized cancer cells to MAPKi exposure.Specifically,we discovered a novel protein complex,HDGF-LGR5,that adaptively responded to MAPKi to enhance cancer cell stemness,which was up-or downregulated by the inhibitors of ITGB3+JNK or ITGB3+IGF1R.Conclusions:Pair-wise sgRNA library screening provided systematic insights into elucidating MAPKi resistance in cancer cells.ITGB3-+IGF1R-targeting drugs(cilengitide+linsitinib)could be used as an effective therapy for suppressing the adaptive formation of the HDGF-LGR5 protein complex,which enhanced cancer stemness during MAPKi stress.

关键词： Pair-wise sgRNA library genetic interactions MAPKi resistance combinatorial therapy cancer stemness

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Carrier-free nanodrugs for stemness inhibition-enhanced photodynamic therapy

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聚集体(英文) 2023年第3期4卷 84-93页

作者： Yuwei Liu Kaiqi Long Tianyi Wang Weirong Kang Weiping Wang State Key Laboratory of Pharmaceutical Biotechnology The University of Hong KongHong KongChina Department of Pharmacology and Pharmacy Li Ka Shing Faculty of MedicineThe University of Hong KongHong KongChina Laboratory of Molecular Engineering and Nanomedicine Dr.Li Dak-Sum Research CentreThe University of Hong KongHong KongChina

cancer stem cell(CSC)has been considered a key driver of tumor growth,recurrence,and metastasis due to its self-renewal and tumor initiation capacities called stemness.stemness is also responsible for the high resistance of CSC to current therapeutic strategies,including photodynamic therapy(PDT)and chemotherapy.In this study,a carrier-free nanodrug(designated as MKCe6 nanoparticle[NP])selfassembled by photosensitizer chlorin e6(Ce6)and stemness inhibitor MK-0752 was prepared for effective tumor repression.stemness inhibition caused by MK-0752 could sensitize CSCs to PDT.Benefiting from the high drug-loading capacity and efficient cellular internalization,MKCe6 NPs exhibited good performance in PDT and stemness inhibition.In this way,effective tumor growth repression and tumorigenesis inhibition by MKCe6 NPs were observed both in vitro and in vivo.This self-delivery nanodrug for stemness inhibition-enhanced photodynamic therapy may provide new insights for clinical cancer therapy.

关键词： cancer stemness nanomedicine Notch pathway photodynamic therapy self-assembly

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Roles of conventional and complementary therapies in recurrent hepatocellular carcinoma

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World Journal of Gastrointestinal Oncology 2023年第1期15卷 19-35页

作者： Hsiang-Chun Lai Hung-Jen Lin Long-Bin Jeng Sheng-Teng Huang Graduate Institute of Chinese Medicine School of Chinese MedicineCollege of Chinese MedicineChina Medical UniversityTaichung 40447Taiwan Department of Chinese Medicine China Medical University HospitalTaichung 40447Taiwan Organ Transplantation Center China Medical University HospitalTaichung 40447Taiwan School of Chinese Medicine China Medical UniversityTaichung 40447Taiwan cancer Research Center for Traditional Chinese Medicine Department of Medical ResearchChina Medical University HospitalTaichung 40447Taiwan An-Nan Hospital China Medical UniversityTainan 709204Taiwan

Hepatocellular carcinoma(HCC)is the fifth most common type of cancer and the fourth leading cause of cancer-related deaths in the world.HCC has a reported recurrence rate of 70%-80%after 5 years of follow-up.Controlling tumor recurrence is the most critical factor associated with HCC mortality.Conventional salvage therapies for recurrent HCC include re-hepatectomy or liver transplantation,transcatheter arterial chemoembolization,Y-90,target therapy,and immunotherapy;however,these conventional treatment modalities have yet to achieve consistently favorable outcomes.Meanwhile,previous studies have demonstrated that conventional therapies in combination with traditional Chinese medicine(TCM),acupuncture,moxibustion or dietary supplements could notably benefit patients with HCC recurrence by strengthening and augmenting the overall management strategy.However,systemic reviews related to the interactions between complementary therapies and conventional therapy in recurrent HCC are limited.In this review,we discuss the molecular mechanisms underlying the functions of complementary therapies for recurrent HCC,which include augmenting the local control to improve the congestion status of primary tumors and reducing multicentric tumor occurrence via inducing autophagy,apoptosis or cell cycle arrest.TCM and its derivatives may play important roles in helping to control HCC recurrence by inhibiting epithelial-mesenchymal transition,migration,invasion,and metastasis,inhibiting cancer stem cells,and ameliorating drug resistance.

关键词： Recurrence Hepatocellular carcinoma Complementary therapy Traditional Chinese medicine cancer stemness Drug resistance

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CAFs shape myeloid-derived suppressor cells to promote stemness of intrahepatic cholangiocarcinoma via 5-lipoxygenase

CAFs shape myeloid-derived suppressor cells to promote stemn...

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第十四届全国免疫学学术大会

作者： Yuli Lin Qian Cai Yu Chen Tiancong Shi Weiren Liu Li Mao Bo Deng Zhen Ying Yuan Gao Haoyang Luo Xuguang Yang Xiaowu Huang Yinghong Shi Rui He Fudan University Key Laboratory of Carcinogenesis and cancer Invasion of Ministry of Education Department of Liver SurgeryLiver Cancer Institute Zhongshan Hospital Shanghai Ninth People's Hospital School of Medicine Shanghai Jiaotong University Department of Oncology Cancer Institute Longhua Hospital Shanghai University of Traditional Chinese Medicine

Background: and Aims: We previously demonstrated that cancer-associated fibroblasts(CAFs) promote tumor growth via recruiting of myeloid-derived suppressor cells(MDSCs). 5-lipoxygenase(5-LO) is highly expressed in myeloid cells and critical for synthesizing leukotriene B4(LTB4), which is involved in tumor progression via activating its receptor Leukotriene B4 receptor type 2(BLT2). In this study, we investigated the potential role of CAFs in regulating MDSC function to enhance cancer stemness, the driving force of the cancer aggressiveness and chemotherapy refractoriness, in highly desmoplastic intrahepatic cholangiocarcinoma(ICC).Approach and Results: RNA-sequencing analysis revealed enriched metabolic pathways but decreased inflammatory pathways in cancer MDSCs compared with blood MDSCs from ICC patients. Co-injection of ICC patient-derived CAFs promoted cancer stemness in an orthotopic ICC model, which was blunted by MDSC depletion. Conditioned media(CM) from CAF-educated MDSCs drastically promoted tumorsphere formation efficiency and stemness marker gene expression in ICC cells. CAF-CM stimulation increased expression and activity of 5-LO in MDSCs while 5-LO inhibitor impaired the stemness-enhancing capacity of MDSCs in vitro and in vivo. Furthermore, CAFs were identified as the major source for IL-6 and IL-33, which mediated hyperactivated 5-LO metabolism in MDSCs. Furthermore, IL-6 and IL-33 mainly expressed by CAFs mediated hyperactivated 5-LO metabolism in MDSCs.We identify the LTB4-BLT2 axis as the critical downstream metabolite signaling of 5-LO in promoting cancer stemness, as treatment with LTB4 that were elevated in CAF-educated MDSCs or blockade of BLT2 that was preferentially expressed in stem-like ICC cells significantly reduced stemness-enhancing effects of CAF-educated MDSCs. Finally, BLT2 blockade augmented chemotherapeutic efficacy in ICC patient derived-xenograft(PDX) models.Conclusions: Our study reveals a previously unrecognized role for CAFs in orchestrating the optimal cancer stemness-enh

关键词： cancer-associated fibroblasts myeloid-derived suppressor cells cancer stemness leukotriene intrahepatic cholangiocarcinoma

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