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miR-221/222 activate the wnt/β-catenin signaling to promote triple-negative breast cancer

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Journal of Molecular Cell Biology 2018年第4期10卷 302-315页

作者： Sanhong Liu Zifeng Wang Zukai Liu Shuo Shi Zhaoran Zhang Jiawei Zhang Haifan Lin Shanghai Institute of Advanced Immunochemical Studies ShanghaiTech University Shanghai China School of Life Science and Technology ShanghaiTech University Shanghai China The Yale Stem Cell Center and Department of Cell Biology Yale University School of Medicine New Haven CT USA

Triple-negative breast cancer （TNBC）, characterized by the lack of expression of the estrogen receptor, the progesterone receptor, and the human epidermal growth factor receptor 2, is an aggressive form of cancer that conveys unpredictable and poor prognosis due to limited treatment options and lack of effective targeted therapies. wnt/β-catenin signaling is hyperactivated in TNBC, which promotes the progression of TNBC. However, the molecular mechanism of wnt/β-catenin activation in TNBC remains unknown. Here, we report the drastic overexpression of miR-221/222 in all of four TNBC cell lines and TNBC primary tumor samples from patients. Furthermore, we demonstrate by both ex vivo and xenograft experiments that inhibiting miR-221/222 expression in a TNBC cell line （MDA-MB-231） suppresses its proliferation, viability, epithelial-to-mesenchymal transition, and migration; whereas expressing miR-221/222 in a non-TNBC line （MCF7） promotes all of the above cancer properties. miR-221/222 achieve so by directly repressing multiple negative regulators of the wnt/β-catenin signaling pathway, including WIF1, SFRP2, DKK2, and AXIN2, to activate the pathway. Notably, the level of miR-221/222 expression is inversely correlated whereas that of WIF1, DKK2, SFRP2, and AXIN2 expression is positively correlated with the patient survival. Last, we show that anti-miR-221/222 significantly increases apoptotic cells with tamoxifen/wnt3a treatment but not with cyclophosphamide/wnt3a treatment. These results demonstrate that miR-221/222 activate the wnt/β-catenin signaling to promote the aggressiveness and TNBC properties of breast cancers, and thus reveal a new prospect for TNBC treatment.

关键词： miR-221/222 wnt/β-catenin triple-negative breast cancer

HYD-PEP06 suppresses hepatocellular carcinoma metastasis,epithelial-mesenchymal transition and cancer stem cell-like properties by inhibiting PI3K/AKT and wnt/β-catenin signaling activation

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Acta Pharmaceutica Sinica B 2021年第6期11卷 1592-1606页

作者： Wei Tian Jiatong Li Zhuo Wang Tong Zhang Ying Han Yanyan Liu Wenfeng Chu Yu Liu Baofeng Yang Department of Pharmacology(the State-Province Key Laboratories of Biomedicine Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China The First Affiliated Hospital of Harbin Medical University Harbin 150081China Translational Medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbin 150081China

HYD-PEP06,an endostatin-modified polypeptide,has been shown to produce effective anticolorectal carcinoma effects through inhibiting epithelial-mesenchymal transition(EMT).However,whether HYD-PEP06 has similar suppressive effect on hepatocellular carcinoma(HCC) remained *** this study,HYD-PEP06 inhibited metastasis and EMT but not proliferation in *** finder pathway reporter array and Western blot analysis revealed that HYD-PEP06 suppressed HCCLM3 cell metastasis and EMT by inhibiting the PI3 K/AKT ***,HYD-PEP06 exerted antimetastasis effects in HepG2 cancer stem-like cells(CSCs) via suppressing the wnt/β-catenin signaling ***,in HCCLM3 tumor-bearing BALB/c nu/nu nude mice,HYD-PEP06 substantially suppressed tumor growth,lung metastasis and HCC *** results suggest that HYD-PEP06 inhibits the metastasis and EMT of HCC and CSCs as well,and thus has the potential as an agent for HCC treatment.

关键词： Hepatocellular carcinoma HYD-PEP06 Cancer stem-like cell PI3K/AKT wnt/β-catenin

wnt/β-catenin signaling in urothelial carcinoma of bladder

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World Journal of Nephrology 2019年第5期8卷 83-94页

作者： Minal Garg Niharika Maurya Department of Biochemistry University of Lucknow

Urothelial carcinoma of bladder is the second most prevalent genitourinary *** is a highly heterogeneous disease as it represents a spectrum of neoplasms,including non-muscle invasive bladder cancer(NMIBC),muscle invasive bladder cancer(MIBC)and metastatic ***-wide approaches and candidate gene analysis suggest that malignant transformation of the bladder is multifactorial and a multitude of genes are involved in the development of MIBC or NMIBC *** signaling is being examined to control and maintain balance between stemness and differentiation in adult stem cell *** to its participation in urothelial development and maintenance of adult urothelial tissue homeostasis,the components of wnt signaling are reported as an important diagnostic and prognostic markers as well as novel therapeutic ***/epigenetic alterations in the key molecules of wnt/β-catenin canonical pathway have been linked with tumorigenesis,development of drug resistance and enhanced *** review extends our understanding on the functions of key regulatory molecules of canonical wnt/β-catenin pathway in urothelial tumorigenesis by inducing cancer stem cell phenotype(UCSCs).UCSCs may be responsible for tumor heterogeneity,high recurrence rates and complex biological behavior of bladder ***,understanding the role of UCSCs and the regulatory mechanisms that are responsible for high relapse rates and metastasis could help to develop pathway inhibitors and augment current *** implications in the treatment of urothelial carcinoma of bladder by targeting this pathway primarily in UCSCs as well as in bulk tumor population that are responsible for high relapse rates and metastasis may facilitate potential therapeutic avenues and better prognosis.

关键词： Chemoresistance Therapeutic approaches Urothelial carcinoma of bladder Urothelial cancer stem cells wnt/β-catenin

Ubiquitin-like modifier activating enzyme 2 promotes cell migration and invasion through wnt/β-catenin signaling in gastric cancer

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World Journal of Gastroenterology 2018年第42期24卷 4773-4786页

作者： Ji Li Xun Sun Ping He Wan-Qi Liu Ya-Bin Zou Quan Wang Xiang-Wei Meng Department of Gastroenterology The First Hospital of Jilin University Department of Pathology The First Hospital of Jilin University Gastrointestinal Surgery The First Hospital of Jilin University

AIM To investigate the function and mechanism of ubiquitinlike modifier activating enzyme 2(Uba2) in progression of gastric cancer(GC) *** Uba2 level in patients with GC was analyzed by Western blotting and immunohistochemistry. MTT and colony formation assays were performed to examine cell *** cytometry was used for cell cycle *** healing and Transwell assays were conducted to examine the effects of Uba2 on migration and *** levels of cell cycle-related proteins, epithelial-mesenchymal transition(EMT) biomarkers, and involvement of the wnt/β-catenin pathway was assessed by Western blotting. Activation of the wnt/β-catenin pathway was confirmed by luciferase *** Uba2 expression was higher in GC than in normal *** Uba2 expression was correlated with tissue differentiation, Lauren's classification, vascular invasion,and TNM stage, as determined by the analysis of 100 GC cases(P wnt/β-catenin signaling pathway as a possible modulator of Uba2 oncogenic *** Uba2 plays a vital role in GC cell migration and invasion,possibly by regulating the wnt/β-catenin signaling pathway and EMT.

关键词： Ubiquitin-like modifier activating enzyme 2 Gastric cancer Epithelial-mesenchymal transition wnt/β-catenin signaling pathway

Alantolactone inhibits proliferation,metastasis and promotes apoptosis of human osteosarcoma cells by suppressing wnt/β-catenin and MAPKs signaling pathways

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Genes & Diseases 2022年第2期9卷 466-478页

作者： Chunmei Yang Lulu Zhang Huakun Huang Xiaohui Yuan Ping Zhang Caihong Ye Mengqi Wei Yanran Huang Xiaoji Luo Jinyong Luo School of Laboratory Medicine Chongqing Medical UniversityChongqing 400016PR China Department of Orthopedics The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400042PR China

Although there are many therapeutic strategies such as surgery and chemotherapy,the prognosis of osteosarcoma(OS)is still far from being *** is urgent to develop more effective,tolerable and safe drugs for the treatment of *** the present study,we investigated the anti-OS activity of Alantolactone(ALT),a natural eucalyptone sesquiterpene lactone mainly exists in Inula helenium,and probed the possible mechanism *** demonstrated that ALT significantly inhibited cell proliferation of various human OS cell lines while had relative lower cytotoxicity against normal ***,we validated that ALT reduced migration,decreased invasion possibly through reversing epithelial mesenchymal transition(EMT)process and suppressing Matrix metalloproteinases(MMPs).Moreover,we confirmed that ALT promoted apoptosis and arrested cell cycle at G2/M phase of human OS cells in *** addition,we confirmed that ALT restrained tumor growth and metastasis of OS 143 cells in a xenograft model in ***,ALT inhibited the activity of wnt/β-catenin and p38,ERK1/2 and JNK Mitogen Activated Protein Kinases(MAPKs)signal ***,the combination of ALT and wnt/β-catenin inhibitor,as well as the combination of ALT and MAPKs inhibitors resulted in a synergistically effect on inhibiting the proliferation,migration and invasion of OS ***,our results validate the ALT may inhibit proliferation,metastasis and promotes apoptosis of human OS cells possibly through suppressing wnt/β-catenin and MAPKs signaling pathways.

关键词： Alantolactone ERK1/2 JNK Mitogen activated protein kinases Osteosarcoma p38 wnt/β-catenin

Echinatin inhibits tumor growth and synergizes with chemotherapeutic agents against human bladder cancer cells by activating p38 and suppressing wnt/β-catenin pathways

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Genes & Diseases 2024年第2期11卷 1050-1065页

作者： Xiaoxuan Wang Lijuan Luo Jingtao Xu Qiuping Lu Haichao Xia Yanran Huang Lulu Zhang Liping Xie Habu Jiwa Shiqiong Liang Xiaoji Luo Jinyong Luo Key Laboratory of Diagnostic Medicine Designated By the Chinese Ministry of Education School of Laboratory MedicineChongqing Medical UniversityChongqing 400016China Department of Orthopedics The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400042China

Bladder cancer (BC) is one of the most common malignant tumors in the urinary *** to the poor prognosis and high mortality rate of the disease,it is urgent to develop new drugs with high efficacy and low toxicity to treat *** (Ecn) is a bioactive natural flavonoid oflicorice that has attracted special attention for its promising anti-tumor ***,we explored the inhibitory effects of Echinatin on BC cells and probed the possible molecular *** found that Ecnin vitro inhibited the proliferation,migration,and invasion,arrested the cell cycle at the G2/M phase,and promoted apoptosis in BC ***,Ecn had no notable cytotoxicity towards human normal *** subsequently confirmed that Ecn restrained xenograft tumor growth and metastasis of BC cells in vivo .Mechanistically,Ecn activated the p38 signaling pathway but inactivated the wnt/β-catenin signaling pathway,while over-expression of β-catenin and the p38 inhibitor both attenuated the inhibitory effects of Ecn on BC ***,Ecn combined with cisplatin (DDP) or gemcitabine (Gem) had synergistic inhibitory effects on BC *** summary,our results validate that Ecn inhibits the tumor growth of human BC cells via p38 and wnt/β-catenin signaling *** meaningfully,our results suggest a potential strategy to enhance DDP- or Gem-induced inhibitory effects on BC cells by combining with Ecn.

关键词： Bladder cancer Combination chemotherapy Echinatin p38 wnt/β-catenin

Stromal cell-derived factor-1α regulates chondrogenic differentiation via activation of the wnt/β-catenin pathway in mesenchymal stem cells

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World Journal of Stem Cells 2023年第5期15卷 490-501页

作者： Xiao Chen Xia-Ming Liang Jia Zheng Yong-Hui Dong Department of Orthopedics Henan Provincial People’s HospitalZhengzhou University People’s HospitalZhengzhou 450003Henan ProvinceChina

BACKGROUND Mesenchymal stem cells(MSCs)have been applied to treat degenerative articular diseases,and stromal cell-derived factor-1α(SDF-1α)may enhance their therapeutic ***,the regulatory effects of SDF-1αon cartilage differentiation remain largely *** the specific regulatory effects of SDF-1αon MSCs will provide a useful target for the treatment of degenerative articular *** To explore the role and mechanism of SDF-1αin cartilage differentiation of MSCs and primary *** The expression level of C-X-C chemokine receptor 4(CXCR4)in MSCs was assessed by *** treated with SDF-1αwere stained for alkaline phosphatase(ALP)and with Alcian blue to observe *** blot analysis was used to examine the expression of SRY-box transcription factor 9,aggrecan,collagen II,runt-related transcription factor 2,collagen X,and matrix metalloproteinase(MMP)13 in untreated MSCs,of aggrecan,collagen II,collagen X,and MMP13 in SDF-1α-treated primary chondrocytes,of glycogen synthase kinase 3β(GSK3β)p-GSK3βandβ-catenin expression in SDF-1α-treated MSCs,and of aggrecan,collagen X,and MMP13 in SDF-1α-treated MSCs in the presence or absence of ICG-001(SDF-1αinhibitor).RESULTS Immunofluorescence showed CXCR4 expression in the membranes of *** stain was intensified in MSCs treated with SDF-1αfor 14 *** SDF-1αtreatment promoted expression of collagen X and MMP13 during cartilage differentiation,whereas it had no effect on the expression of collagen II or aggrecan nor on the formation of cartilage matrix in ***,those SDF-1α-mediated effects on MSCs were validated in primary ***-1αpromoted the expression of p-GSK3βandβ-catenin in ***,finally,inhibition of this pathway by ICG-001(5μmol/L)neutralized the SDF-1α-mediated up-regulation of collagen X and MMP13 expression in *** SDF-1αmay promote hypertrophic cartilage differentiation in MSCs by activating the wnt/β-caten

关键词： Stromal cell-derived factor-1α Mesenchymal stem cells Chondrogenic differentiation wnt/β-catenin C-X-C chemokine receptor 4

Mechanism of annexin A1/N-formylpeptide receptor regulation of macrophage function to inhibit hepatic stellate cell activation through wnt/β-catenin pathway

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World Journal of Gastroenterology 2023年第22期29卷 3422-3439页

作者： Jun-Hua Fan Na Luo Geng-Feng Liu Xiao-Fang Xu Shi-Quan Li Xiao-Ping Lv Department of Gastroenterology The First Affiliated Hospital of Guangxi Medical UniversityNanning 530021Guangxi Zhuang Autonomous RegionChina

BACKGROUND Hepatic fibrosis is a common pathological process of chronic liver diseases with various causes,which can progress to *** To evaluate the effect and mechanism of action annexin(Anx)A1 in liver fibrosis and how this could be targeted *** CCl4(20%)and active N-terminal peptide of AnxA1(Ac2-26)and N-formylpeptide receptor antagonist N-Boc-Phe-Leu-Phe-Leu-Phe(Boc2)were injected intraperitoneally to induce liver fibrosis in eight wild-type mice/Anxa1 knockout mice,and to detect expression of inflammatory factors,collagen deposition,and the role of the wnt/β-catenin pathway in hepatic *** Compared with the control group,AnxA1,transforming growth factor(TGF)-β1,interleukin(IL)-1βand IL-6 expression in the liver of mice with hepatic fibrosis induced by CCl4 was significantly increased,which promoted collagen deposition and expression ofα-smooth muscle actin(α-SMA),collagen type I and connective tissue growth factor(CTGF),and increased progressively with ***4 induced an increase in TGF-β1,IL-1βand IL-6 in liver tissue of AnxA1 knockout mice,and the degree of liver inflammation and fibrosis and expression ofα-SMA,collagen I and CTGF were significantly increased compared with in wild-type *** treatment with Ac2-26,expression of liver inflammatory factors,degree of collagen deposition and expression of a-SMA,collagen I and CTGF were decreased compared with before ***2 inhibited the anti-inflammatory and antifibrotic effects of ***1 downregulated expression of the wnt/β-catenin pathway in CCl4-induced hepatic *** vitro,lipopolysaccharide(LPS)induced hepatocyte and hepatic stellate cell(HSC)expression of ***2-26 inhibited LPS-induced RAW264.7 cell activation and HSC proliferation,decreased expression ofα-SMA,collagen I and CTGF in HSCs,and inhibited expression of the wnt/β-catenin pathway after HSC *** therapeutic effects were inhibited by *** AnxA1 inhibited

关键词： Annexin A1 Active N-terminal peptide of annexin A1 Macrophage Hepatic stellate cell wnt/β-catenin Liver fibro

Role of wnt/β-catenin Pathway in the Arterial Medial Calcification and Its Effect on the OPG/RANKL System

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Current Medical Science 2019年第1期39卷 28-36页

作者： Bin NIE Shao-ying ZHANG Si-ming Guan Shao-qiong ZHOU Xin FANG Department of Geriatrics the Central Hospital of WuhanTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430014China Department of Geriatrics Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China

In this study,the hypothesis that wnt/β-catenin pathway is involved in the arterial calcification by regulating the osteoprotegerin(OPG)/receptor activator of NF-κB ligand(RANKL)system was ***β-catenin expression was measured in the warfarin-induced calcified arteries and the osteoblast-like cells differentiating from smooth muscle cells(SMCs)by immunohistochemistry and Western *** wnt/β-catenin pathway was activated or inhibited by lithium chloride(LiCl)or dickkopf 1(DKK1)in vitro and in *** the calcification level was determined by von Kossa staining,Ca^2+content assay,and alkaline phosphatase(ALP)activity *** expression levels of osteocalcin,OPG and RANKL were detected by Western blotting or real-time *** results showed that in calcified arteries and OBL cells,the activation of wnt/β-catenin pathway significantly enhanced the calcification as evidenced by increased von Kossa stains,Ca^2+contcnts,ALP activities,and osteocalcin expression levels(Pwnt/β-catenin pathway worsens the arterial calcification,probably by promoting the RANKL expression.

关键词： arterial calcification wnt/β-catenin pathway osteoprotegerin receptor activator of NF-κB ligand