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| 1 | PEITC triggers multiple forms of cell death by GSH-iron-ROS regulation in K7M2 murine osteosarcoma cells显示文摘Phenethyl isothiocyanate(PEITC)is an isothiocyanate that largely exists in cruciferous vegetables and exhibits chemopreventive and chemotherapeutic potential against various cancers.However,it is little known about the molecular mechanisms of its antitumor action against osteosarcoma,which is the second highest cause of cancer-related death in children and adolescents.In this study,we investigated the effects of PEITC on K7M2murine osteosarcoma both in vitro and in vivo.We found that treatment with PEITC dose-dependently inhibited the viability of K7M2 murine osteosarcoma cells with an lCso value of 33.49μM at 24h.PEITC(1,15,30μM)dose-dependently inhibited the cell proliferation,caused G/M cell cycle arrest,depleted glutathione(GSH)generated reactive oxygen species(ROS),altered iron metabolism,and triggered multiple forms of cell death,namely ferroptosis apoptosis,and autophagy in K7M2 cells.We further revealed that PEITC treatment activated MAPK signaling pathway,and ROS generation was a major cause ofPEITC-induced cell death.In a syngeneic orthotopic osteosarcoma mouse model,administration of PEITC(30,60 mg/kg every day,ig,for 24 days)significantly inhibited the tumor growth,but higher dose of PEITC(90 mg/kg every day)compromised its ant-osteosarcoma effect.Histological examination showed that multiple cell death processes were initiated,iron metabolism was altered and MAPK signaling pathway was activated in the tumor tissues.In conclusion,we demonstrate that PEITC induces ferroptosis,autophagy,and apoptosis in K7M2 osteosarcoma cell by activating the ROS-elated MAPK signaling pathway.PEITC has promising anti-osteosarcoma activity.This study sheds light on,the redox signaling-based chemotherapeutics for cancers. | Huan-huan Lv Chen-xiao Zhen Jun-yu Liu Peng Shang | 2020 | Acta Pharmacologica Sinica2020，41，8： | 12 |
| 2 | Isolation and Identification of Cancer Stem Cells from Human Osteosarcom by Serum-free Three-dimensional Culture Combined with Anticancer Drugs显示文摘The cancer stem cells(CSCs)from human osteosarcoma by serum-free three-dimensional culture combined with anticancer drugs were isolated and identified.The primary cells derived from human osteosarcoma were digested by trypsin to prepare a single-cell suspension,and mixed homogeneously into 1.2% alginate gel.Single-cell alginate gel was cultured with serum-free DMEM/F12 medium.Epirubicin(0.8μg/mL)was added to the medium to enrich CSCs.After cultured conventionally for 7 to 10 days,most of cells suspended in alginate gel were killed by epirubicin.But few cells survived and some single-cell cloning spheres formed.Immunofluorescent staining for Oct3/4 and Nanog was implemented to find cells with properties of self-renewal and multi-potential differentiation.Cells from cloning spheres were transplanted into BALB/c mice to detect the tumorigenicity in vivo.The results showed that some cells positive for Oct3/4(TRITC)and Nanog(TRITC)were found in single-cell cloning spheres,and most of positive cells were concentrated in the core of sphere.Cells from spheres could form osteosarcoma in the body of mice.It was concluded that cells from single-cell cloning spheres had the properties of the expression of parts of stem cell genes(Oct3/4 and Nanog),resisting anti-cancer drugs,and tumorigenicity in vivo.To sum up,it is believed that cells obtained from osteosarcoma by serum-free three-dimensional culture combined with anticancer drugs are cancer stem cells. | 周松 李锋 肖骏 熊伟 方忠 陈文坚 牛鹏彦 | 2010 | Journal of Huazhong University of Science and Technology(Medical Sciences)2010，30，1： | 7 |
| 3 | KIF18B promotes tumor progression in osteosarcoma by activating β-catenin显示文摘Objective:Osteosarcoma is a common primary highly malignant bone tumor.Kinesin family member 18B(K1F18B)has been identified as a potential oncogene involved in the development and metastasis of several cancer types.While KIF18B overexpression in osteosarcoma tissue is clearly detected,its specific function in the disease process remains to be established.Methods:K IF18B expression was assessed in osteosarcoma tissues and cells.We additionally evaluated the effects of KIF18B on proliferation,migration,and invasion of osteosarcoma cells,both in vitro and in vivo.Results:Our results showed overexpression of KIF18B in osteosarcoma tissues and cells.Knockdown of K IF18B induced G1/S phase arrest and significantly inhibited proliferation,migration,and invasion of osteosarcoma cells,both in vitro and in vivo.K IF18B regulated P-catenin expression at the transcriptional level by controlling nuclear aggregation of ATF2 and at the post-transcriptional level by interacting with the adenomatous polyposis coli(APC)tumor suppressor gene in osteosarcoma cells.Conclusions:KIF18B plays a carcinogenic role in osteosarcoma by regulating expression ofβ-catenin transcriptionally via decreasing nuclear aggregation of ATF2 or post-transcriptionally through interactions with APC.Our collective findings support the potential utility of KIF18B as a novel prognostic biomarker for osteosarcoma. | Tian Gao Ling Yu Zhiwei Fang Jiayong Liu Chujie Bai Shu Li Ruifeng Xue Lu Zhang Zhichao Tan Zhengfu Fan | 2020 | Cancer Biology & Medicine2020，17，2： | 7 |
| 4 | miRNA-296-5p functions as a potential tumor suppressor in human osteosarcoma by targeting SND1显示文摘Background:The pathogenesis of osteosarcoma(OS)is still unclear,and it is still necessary to find new targets and drugs for anti-OS.This study aimed to investigate the role and mechanism of the anti-OS effects of miR-296-5p.Methods:We measured the expression of miR-296-5p in human OS cell lines and tissues.The effect of miR-296-5p and its target gene staphylococcal nuclease and tudor domain containing 1 on proliferation,migration,and invasion of human OS lines was examined.The Student's t test was used for statistical analysis.Results:We found that microRNA(miR)-296-5p was significantly downregulated in OS cell lines and tissues(control vs.OS,1.802±0.313 i/s.0.618±0.235,f=6.402,P<0.01).Overexpression of miR-296-5p suppressed proliferation,migration,and invasion of OA cells.SND1 was identified as a target of miR-296-5p by bioinformatic analysis and dual-luciferase reporter assay.Overexpression oiSNDl abrogated the effects induced by miR-296-5p upregulation(miRNA-296-5p vs.miRNA-296-5p+SND1,0.294±0.159 t/s.2.300±0.277,t=12.68,P=0.003).Conclusion:Our study indicates that miR-296-5p may function as a tumor suppressor by targeting SND1 in OS. | Ya-Zeng Huang Jun Zhang Jian-Jian Shen Ting-Xiao Zhao You-Jia Xu | 2021 | Chinese Medical Journal2021，，5： | 7 |
| 5 | Inhibition of M2-like macrophages by all-trans retinoic acid prevents cancer initiation and sternness in osteosarcoma cells显示文摘Emerging evidence indicates that M2-polarized tumor-associated macrophages(TAMs)directly participate in tumor initiation,progression and metastasis.However,to date,few studies have investigated novel strategies for inhibiting TAMs in order to overcome osteosarcoma.In this study,we reported that M2 macrophages were enriched in osteosarcoma tissues from patients,and M2-polarized TAMs enhanced cancer initiation and sternness of osteosarcoma cells,thereby establishing M2-polarized TAMs as a therapeutic target for blocking osteosarcoma formation.We also found that all-trans retinoic acid(ATRA)weakened TAM-induced osteosarcoma tumor formation by inhibiting M2 polarization of TAMs in vivo,and inhibited the colony formation,as well as sphereformation capacity of osteosarcoma cells promoted by M2-type macrophages in vitro.Furthermore,M2-type macrophages enhanced cancer stem cells(CSCs)properties as assessed by increasing the numbers of CD117+Stro-1+cells accompanied by the upregulation of CSC markers(CD133,CXCR4,Nanog,and Oct4),which could clearly be reduced by ATRA.Taken together,the results of this study demonstrated the role of M2-polarized TAMs in osteosarcoma initiation and sternness by activating CSCs,and indicated that ATRA treatment is a promising approach for treating osteosarcoma by preventing M2 polarization of TAMs. | Xue-jing Shao Sen-feng Xiang Ying-qian Chen Ning Zhang Ji Cao Hong Zhu Bo Yang Qian Zhou Mei-dan Ying Qiao-jun He | 2019 | Acta Pharmacologica Sinica2019，40，10： | 6 |
| 6 | Perioperative rh-endostatin with chemotherapy improves the survival of conventional osteosarcoma patients: a prospective non-randomized controlled study显示文摘Objective: Anti-angiogenic drugs are an emerging treatment option against malignant tumors. The aim of this study was to determine whether the addition of perioperative rh-endostatin to chemotherapy could improve the probability of distant metastasis-free survival(DMFS) and overall survival(OS) in patients newly diagnosed with non-metastatic conventional osteosarcoma.Methods: This was a controlled non-randomized clinical study that included 388 patients without clinically detectable metastatic disease enrolled from January 2008 to April 2012. The control treatment group had 272 patients; 180 were male and 92, female,with a median age of 17 years. The treatment group had 58 patients; 36 were male and 22, female, with a median age of 16 years.The control group received preoperative chemotherapy followed by surgery and postoperative chemotherapy. The treatment group received 4 cycles of rh-endostatin perioperatively in addition to chemotherapy as per the control group. Patients were followed up from 6-101 months with a median follow-up period of 50.2 months.Results: The 5-year DMFS of the control group(61%) was significantly lower than that of the rh-endostatin group(79%)(P = 0.013). The 5-year OS of the control group(74%) was significantly lower than that of the rh-endostatin treatment group(87%)(P = 0.029). No difference in adverse drug reactions was found between these 2 groups.Conclusions: The addition of perioperative rh-endostatin to chemotherapy could significantly improve the DMFS and OS of patients with non-metastatic osteosarcoma. | Hairong Xu Zhen Huang Yuan Li Qing Zhang Lin Hao Xiaohui Niu | 2019 | Cancer Biology & Medicine2019，16，1： | 5 |
| 7 | Wnt signaling and Loxl2 promote aggressive osteosarcoma显示文摘Osteosarcoma(OS)is the most frequent primary malignant bone tumor in urgent need of better therapies.Using genetically modified mouse models(GEMMs),we demonstrate that Wnt signaling promotes c-Fos-induced OS formation via the actions of the collagen-modifying enzyme Loxl2.c-Fos/AP-1 directly regulates the expression of the Wnt ligands Wnt7b and Wnt9a in OS cells through promoter binding,and Wnt7b and Wnt9a in turn promote Loxl2 expression in murine and human OS cells through the transcription factors Zeb1 and Zeb2.Concordantly,inhibition of Wnt ligand secretion by inactivating the Wnt-less(Wls)gene in osteoblasts in c-Fos GEMMs either early or in a therapeutic setting reduces Loxl2 expression and progression of OS.Wls-deficient osteosarcomas proliferate less,are less mineralized and are enriched in fibroblastic cells surrounded by collagen fibers.Importantly,Loxl2 inhibition using either the pan-Lox inhibitor BAPN or a specific inducible shRNA reduces OS cell proliferation in vitro and decreases tumor growth and lung colonization in murine and human orthotopic OS transplantation models.Finally,OS development is delayed in c-Fos GEMMs treated with BAPN or with specific Loxl2 blocking antibodies.Congruently,a strong correlation between c-FOS,LOXL2 and WNT7B/WNT9A expression is observed in human OS samples,and c-FOS/LOXL2 co-expression correlates with OS aggressiveness and decreased patient survival.Therefore,therapeutic targeting of Wnt and/or Loxl2 should be considered to potentiate the inadequate current treatments for pediatric,recurrent,and metastatic OS. | Kazuhiko Matsuoka Latifa Bakiri Lena I.Wolff Markus Linder Amanda Mikels-Vigdal Ana Patiño-García Fernando Lecanda Christine Hartmann Maria Sibilia Erwin F.Wagner | 2020 | Cell Research2020，30，10： | 5 |
| 8 | KLF4 functions as an oncogene in promoting cancer stem celllike characteristics in osteosarcoma cells显示文摘Despite more effective chemotherapy combined with limb-salvage surgery for the osteosarcoma treatment, survival rates for osteosarcoma patients have stagnated over the past three decades due to the poor prognosis. Osteosarcoma cancer stem cells (OSCs) are responsible for the growth and metastasis of osteosarcoma. The existence of OSCs offers a theoretical explanation for therapeutic failures in cludi ng tumor recurrence, metastasis, and drug resista nee. Un dersta nding the pathways that regulate properties of OSCs may shed light on mechanisms that lead to osteosarcoma and suggest better modes of treatment. In this study, we showed that the expression level of Kruppel-like factor 4 (KLF4) is highly associated with human osteosarcoma cancer stemness. KLF4-overexpressed osteosarcoma cells displayed characteristics of OSCs: in creased sphere-forming pote ntial, enhan ced levels of sternness-associated genes, great chemoresistanee to adriamycin and CDDP, as well as more metastasis potential. Inversely, KLF4 knockdown could reduce colony formation in vitro and inhibit tumorigenesis in vivo, supporting an oncogenic role for KLF4 in osteosarcoma pathogenesis. Furthermore, KLF4 was shown to activate the p38 MAPK signaling pathway to promote cancer stemness. Altogether, our studies uncover an essential role for KLF4 in regulation of OSCs and identify KLF4-p38 MAPK axis as a potential therapeutic target for osteosarcoma treatment. | Xiao-tian Qi Yang-ling Li Yan-qi Zhang Tong Xu Bin Lu Liang Fang Jian-qing Gao Lu-shan Yu Di-feng Zhu Bo Yang Qiao-jun He Mei-dan Ying | 2019 | Acta Pharmacologica Sinica2019，40，4： | 5 |
| 9 | SNHG1 functions as an oncogenic lncRNA and promotes osteosarcoma progression by up-regulating S100A6 viamiR-493-5p显示文摘The mechanism behind the aberrant expression of S100A6 in osteosarcoma is seldom reported so far.This study sought to explore the regulatory axis targeting S100A6 involved in osteosarcoma progression.Clinical samples collected from osteosarcoma patients were used to detect the expressions of SNHG1,miR-493-5p,and S100A6 by western bolt analysis and reverse transcription-quantitative polymerase chain reaction(RT-qPCR).The effects of S100A6 on proliferation and osteogenic differentiation were investigated by the CCK-8 assay,colony formation assay,Ethynyl deoxyuridine staining,matrix mineralization assay,and alkaline phosphatase assay.The potential of lncRNAs/miRNAs targeting S100A6 was identified by the bioinformatics approach,and the results were verified by the dual luciferase assay and RNA immunoprecipitation assay.Both in vitro and in vivo rescue experiments were performed to investigate the regulatory relationship between the identified lncRNAs and S100A6.The results showed that S100A6 is highly expressed in osteosarcoma.S100A6 overexpression not only increases the proliferation but also reduces the osteogenic differentiation of osteosarcoma cells,while S1006A silence exerts the opposite effects.Then,SNHG1 is identified to directly interact with miR-493-5p to attenuate miR-493-5p binding to the 3′-untranslated region of S100A6.Notably,S100A6 silence partially rescues the effect of SNHG1 overexpression on proliferation and osteogenic differentiation of osteosarcoma cells.Furthermore,the suppressive role of SNHG1 silence in the growth of osteosarcoma xenograft tumors is countered by S100A6 overexpression.Collectively,this study reveals that S100A6 plays an important role in osteosarcoma progression,and SNHG1 promotes S100A6 expression by competitively sponging miR-493-5p. | Qi Liu Jiaying Luo Huan Wang Lei Zhang Guoxin Jin | 2022 | Acta Biochimica et Biophysica Sinica2022，54，1： | 5 |
| 10 | The expression of MYH9 in osteosarcoma and its effect on the migration and invasion abilities of tumor cell显示文摘Objective: To determine the expression of non-muscle myosin heavy chain 9(MYH9) in osteosarcoma and its effect on the migration and invasion abilities of tumor cell. Methods: A total of 65 cases of osteosarcoma and 20 cases with benign osteochondroma who underwent resection operation in the Orthopaedics Department of our hospital from January 1st 2009 to January 1st 2015 were selected. Their mR NA levels of MYH9 were tested by q rt-PCR. Immunohistochemical method was used to examine the expression of MYH9 in osteosarcoma and the correlation between the positive expression of MYH9 and the clinicopathological features of patients was illustrated by statistical analysis. MYH9 was compounded artificially. The expression of MYH9 in SAOS2 osteosarcoma cells was decreased by si RNA. Scratch test was used to determine the change of SAOS2 cell migration ability after MYH9 silence. Transwell assay was employed to detect the change of cell invasion ability after MYH9 silence.Results: The expression levels of m RNA of MYH9 and protein in osteosarcoma tissues were significant higher than those in benign osteochondroma tissues. The high expression of MYH9 in osteosarcoma tissues was apparently related to the high Enneking classification(III classification) and lung metastasis. SiR NA of MYH9 could evidently decrease the expression level of MYH9 in SAOS2. The down-regulated expression of MYH9 could inhibit the migration and invasion abilities of SAOS2 cells. Conclusions: MYH9 shows a trend of high expression in osteosarcoma tissues, and its high expression is associated with features such as tumor invasion and metastasis. The down-regulated MYH9 can realize an anti-tumor effect by inhibiting the migration and invasion of osteosarcoma cells. | Wei Zhou Ming-Yu Fan You-Xiu Wei Song Huang Jing-You Chen Ping Liu | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，6： | 5 |
| 11 | Nb2C MXene-Functionalized Scaffolds Enables Osteosarcoma Phototherapy and Angiogenesis/Osteogenesis of Bone Defects显示文摘Early surgical resection and chemotherapy of bone cancer are commonly used in the treatment of bone tumor,but it is still highly challenging to prevent recurrence and fill the bone defect caused by the resection site.In this work,we report a rational integration of photonic-responsive two-dimensional(2D)ultrathin niobium carbide(Nb2C)MXene nanosheets(NSs)into the 3D-printed bone-mimetic scaffolds(NBGS)for osteosarcoma treatment.The integrated 2D Nb2C-MXene NSs feature specific photonic response in the second near-infrared(NIR-II)biowindow with high tissue-penetrating depth,making it highly efficient in killing bone cancer cells.Importantly,Nb-based species released by the biodegradation of Nb2C MXene can obviously promote the neogenesis and migration of blood vessels in the defect site,which can transport more oxygen,vitamins and energy around the bone defect for the reparative process,and gather more immune cells around the defect site to accelerate the degradation of NBGS.The degradation of NBGS provides sufficient space for the bone remodeling.Besides,calcium and phosphate released during the degradation of the scaffold can promote the mineralization of new bone tissue.The intrinsic multifunctionality of killing bone tumor cell and promoting angiogenesis and bone regeneration makes the engineered Nb2C MXeneintegrated composite scaffolds a distinctive implanting biomaterial on the efficient treatment of bone tumor. | Junhui Yin Shanshan Pan Xiang Guo Youshui Gao Daoyu Zhu Qianhao Yang Junjie Gao Changqing Zhang Yu Chen | 2021 | Nano-Micro Letters2021，13，2： | 5 |
| 12 | Reversal of multidrug resistance by icaritin in doxorubicin-resistant human osteosarcoma cells显示文摘Multidrug resistance(MDR) is one of the major obstacles in cancer chemotherapy. Our previous study has shown that icariin could reverse MDR in MG-63 doxorubicin-resistant(MG-63/DOX) cells. It is reported that icariin is usually metabolized to icariside II and icaritin. Herein, we investigated the effects of icariin, icariside Ⅱ, and icaritin(ICT) on reversing MDR in MG-63/DOX cells. Among these compounds, ICT exhibited strongest effect and showed no obvious cytotoxicity effect on both MG-63 and MG-63/DOX cells ranging from 1 to 10 μmol·L^(-1). Furthermore, ICT increased accumulation of rhodamine 123 and 6-carboxyfluorescein diacetate and enhanced DOX-induced apoptosis in MG-63/DOX cells in a dose-dependent manner. Further studies demonstrated that ICT decreased the m RNA and protein levels of multidrug resistance protein 1(MDR1) and multidrug resistance-associated protein 1(MRP1). We also verified that blockade of STAT3 phosphorylation was involved in the reversal effect of multidrug resistance in MG-63/DOX cells. Taken together, these results indicated that ICT may be a potential candidate in chemotherapy for osteosarcoma. | WANG Zhen-Dong WANG Rui-Zhi XIA Yuan-Zheng KONG Ling-Yi YANG Lei | 2018 | Chinese Journal of Natural Medicines2018，16，1： | 5 |
| 13 | Experimental Study on Inhibitory Effects of Diallyl Sulfide on Growth and Invasion of Human Osteosarcoma MG-63 Cells显示文摘The inhibitory effects of diallyl sulfide(DAS) derived from allicin on in vitro and in vivo proliferation of human osteosarcoma MG-63 cells and the action mechanism,and the influence of DAS on invasive capability of MG-63 cells were investigated in order to search for the novel medicines for osteosarcoma.In the in vitro experiment,MG-63 cells were treated with different concentrations of DSA,and the morphological changes of MG-63 cells were observed under an inverted phase microscope.MTT method was used to assay the proliferation of MG-63 cells.Semi-quantitative reverse transcription polymerase chain reaction(RT-PCR) was used to detect the VEGF mRNA expression level in MG-63 cells.By using Transwell invasion assay,the influence of DAS on invasive ability of MG-63 cells was tested.In the in vivo experiment,the nude mice MG-63 cells tumor-bearing model was established,and different concentrations of DAS were injected beside the tumor.Twenty-one days after treatment,the mice were killed,the tumor size and tumor inhibition rate were calculated.The microvessel density(MVD) was determined by using immunohistochemistry.In the in vitro experiment,different concentrations of DAS could obviously inhibit proliferation of MG-63 cells in a time-and concentration-dependent manner.RT-PCR revealed that the expression levels of VEGF mRNA in DSA groups(different concentrations) were significant reduced as compared with those in control group(all P<0.05).Transwell invasion assay indicated that in 20 and 40 μg/mL DAS groups,the number of migratory cells was 91.4±8.3 and 81.8±7.4 respectively,which was significantly declined as compared with that in control group(150.4±14.7,both P<0.05).In the in vivo experiment,DAS could significantly suppress the growth of MG-63 tumor-bearing tissue.Immunohistochemistry demonstrated that different concentrations(20 and 40 μg/mL) of DAS could significantly decrease MVD of MG-63 tumor-bearing tissue(all P<0.05).It was suggested that DAS could inhibit the growth of MG-63 cells probably by suppressing the expression of VEGF mRNA. | 胡友珍 陈玲 易呈志 杨帆 陈继革 | 2012 | Journal of Huazhong University of Science and Technology(Medical Sciences)2012，32，4： | 4 |
| 14 | MMP-1 Over-expression Promotes Malignancy and Stem-Like Properties of Human Osteosarcoma MG-63 Cells In Vitro显示文摘Osteosarcoma is the most common primary malignant bone tumor in childhood,and it maintains a high level of recurrence.Matrix metalloproteinase-1(MMP-1)was found to contribute to cancer progression.The present study was to investigate the in vitro effects of MMP-1 over-expression on the proliferation,invasion,metastasis and stem-like properties of osteosarcoma MG-63 cells.The MG-63 cells were cultured and had a full length MMP-1 cDNA inserted by the tentiviral vector (MG-63^MMP-1+).MG-63 negative control and MG-63 blank control groups were established as well.MMP-1 expression was detected in MG-63^MMP-1+,MG-63 negative control and MG-63 blank control cells using qPCR,Western blotting and immunofluorescence after 24h of culture. The cell proliferation assay was performed with a camera attached to a bioreactor,which was programmed to photograph five regions of each well every 10 min over a period of 48 h.The cell invasion assay was conducted with Matrigel to assess the invasive potential,of MG-63 cells over 24h,the qPCR analysis to measure stem cell markers,including Oct4, Sox-2,Nanog,and Pax-7,and Western blot analysis to detect invasive and metastatic potential markers TIMP-1,VEGF and BMP2/4,after 24h of culture.Immunofluorescence was used to investigate the presence of the stem cell marker Pax-7 after 24-h culture. The results showed that over-expression of MMP-1 after transfection could significantly increase minor cell proliferation and invasion (P<0.05,MG-63^MMP-1+ versus controls).Pax-7 was highly expressed in MG-63^MMP-1+ cells,with no significant changes of Oct-4,Sox-2, and Nanog observed (P<0.05).MG-63^MMP-1+ cells showed higher expression of VEGF and BMP 2/4 proteins and lower expression of TIMP-1 protein than controls (P<0.05).It was concluded that MMP-1 over-expression in MG-63 cells contributed to the proliferation, invasion,metastasis and stem-like properties of osteosarcoma cells.Future studies should focus on in vivo effects of MMP-1 over-expression and the application of MMP-1 and Pax-7 inhibition in vivo to osteosarcoma theraoies. | Man-li TANG Xiang-jun BAI Yong LI Xiao-jing DAI Fan YANG | 2018 | Current Medical Science2018，38，5： | 4 |
| 15 | 肿瘤标志物在骨肉瘤中的研究显示文摘骨肉瘤(osteosarcoma,OS)是最常见的威胁青少年生命健康的高度恶性骨肿瘤[1]。骨肉瘤好发于长骨或者血运供应充足的干骺端,由于实体瘤的组织异质性和对放化疗的耐受性不同,导致骨肉瘤的肺转移率显著升高且预后较差[2]。常规的治疗手段(化学治疗、放射治疗、免疫治疗等生物治疗)很难从根本上治愈骨肉瘤, | 任仰光 尤建宇 张宁 赵宝林 | 2015 | 中国实验诊断学2015，19，11： | 4 |
| 16 | 7,8-Dihydroxyflavone suppresses proliferation and induces apoptosis of human osteosarcoma cells显示文摘Recent studies suggest that 7,8-dihydroxyflavone(7,8-DHF)inhibits the development of several tumors.However,its role in osteosarcoma(OS)remains unknown.This study was designed to investigate the effects and underlying mechanisms of 7,8-DHF that may influence OS development.Human OS cell lines(U2OS and 143B)were treated with 7,8-DHF;cell viability and cell migration were assessed by methylthiazolyldiphenyl-tetrazolium bromide(MTT)assay and wound-healing assay,respectively;and cell death and apoptosis were evaluated by LIVE/DEAD staining and terminal deoxynucleotidyl transferase(TdT)dUTP nick-end labeling(TUNEL)assay,respectively.Reactive oxygen species production was measured using 2,7-dichlorodihydrofluorescein diacetate probe.Akt,Bcl-xL/Bcl-2 asociated death promoter(Bad),p38 mitogen-activated protein kinase(MAPK),extracellular regulated protein kinase(ERK),and c-Jun N-terminal kinase(JNK)expression and their respective phosphorylation levels were detected by western blot analysis.We found that 7,8-DHF reduced cell viability in a dose-dependent manner and also promoted apoptosis,inhibited migration,and induced oxidative stress in OS cells.Moreover,7,8-DHF inhibited Akt,Bad,and p38MAPK,but activated ERK and JNK signals.In summary,our results suggest that 7,8-DHF inhibits OS progression,possibly by regulating Akt/Bad and MAPK signaling.These findings provide new evidence for the pharmacological effects of 7,8-DHF that may improve drug therapy for OS patients. | Jing Zhao Peifeng Li Hua Zhu Fengqin Ge Jie Liu Jingjun Xia Pengzhou Hang | 2021 | Acta Biochimica et Biophysica Sinica2021，53，7： | 3 |
| 17 | miR-218 expression in osteosarcoma tissues and its effect on cell growth in osteosarcoma cells显示文摘Objective:To investigate the expression of miR—218 and its clinical significance in osteosarcoma tissues and explore its effect on proliferation and apoptosis in osteosarcoma cells.Methods:miR-218 expression was detected in 76 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues using quantitative reverse transcription polymerase chain reaction(qRT-PCR).MiR-218 was over-expressed by exogenous miR-218 plasmids in Saos-2 cells,and then BrdU cell proliferation assay and flow cytometry were used to determine cell proliferation and apoptosis.Results:The expression of miR-218 in osteosarcoma tissues was significantly lower than those in normal tumor-adjacent tissues(t=8.735.P<0.001).MiR-218 expression in tumor tissues was significantly correlated with tumor size(x^2=5.380,P=0.020).clinical stage(x^2=6.692,P=0.010) and distant metastasis(x^2=4.l80.P=0.041).MiR-218 was obviously overexpressed by exogenous miR-218 plasmids(t= 19.42.P<0.001),and miR-218 overexpression significantly reduced cell proliferation(t=9.045.P<0.001) and induced apoptosis(t=12.38,P<0.001) in Saos-2 cells.Conclusions:The low-expression of miR-218 is correlated with the poor clinicopathological features in osteosarcoma.Moreover.miR-218 overexpression reduces cancer cell proliferation and induces apoplosis in Saos-2 cells,suggesting that miR-218 may play a key role in the progression of human osteosarcoma. | Hong-Tai Wang Ai-Gang Liu Dao-Shu Luo Zhang-Nan Zhou Hong-Guang Lin Rong-Zi Chen Jin-Shui He Kun Chen | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，12： | 3 |
| 18 | Managing the immune microenvironment of osteosarcoma:the outlook for osteosarcoma treatment显示文摘Osteosarcoma,with poor survival after metastasis,is considered the most common primary bone cancer in adolescents.Notwithstanding the efforts of researchers,its five-year survival rate has only shown limited improvement,suggesting that existing therapeutic strategies are insufficient to meet clinical needs.Notably,immunotherapy has shown certain advantages over traditional tumor treatments in inhibiting metastasis.Therefore,managing the immune microenvironment in osteosarcoma can provide novel and valuable insight into the multifaceted mechanisms underlying the heterogeneity and progression of the disease.Additionally,given the advances in nanomedicine,there exist many advanced nanoplatforms for enhanced osteosarcoma immunotherapy with satisfactory physiochemical characteristics.Here,we review the classification,characteristics,and functions of the key components of the immune microenvironment in osteosarcoma.This review also emphasizes the application,progress,and prospects of osteosarcoma immunotherapy and discusses several nanomedicine-based options to enhance the efficiency of osteosarcoma treatment.Furthermore,we examine the disadvantages of standard treatments and present future perspectives for osteosarcoma immunotherapy. | Hailong Tian Jiangjun Cao Bowen Li Edouard CNice Haijiao Mao Yi Zhang Canhua Huang | 2023 | Bone Research2023，11，1： | 3 |
| 19 | Effect of PI3K-mediated autophagy in human osteosarcoma MG63 cells on sensitivity to the chemotherapy drug cisplatin显示文摘Objective: To investigate the influence of autophagy on sensitivity to the chemotherapy drug cisplatin(DDP) and the role of PI3 K in autophagy. Methods: MTT methods and l ow cytometer, with rapamycin up-regulating the autophagy and 3-MA down-regulating the autophagy, were employed to measure the proliferation inhibition rate on DDP-treated osteosarcoma cells and the change in cell cycle. The expression of intracellular protein was detected by Western blot. The autophagy of MG63 cell was observed using l uorescence microscope and transmission electron microscope. Results: Western blot showed that basic autophagy level of MG63 cell was significantly lower than that of h FOB cell. MTT test revealed that the cell proliferation inhibition rate in the group treated with rapamycin and DDP, group treated with 3-MA and DDP, and group only treated with DDP was signii cantly dif erent. It was demonstrated by the l ow cytometry that in group treated with DDP, inhibition on autophagy can increase the cell numbers in G1 phase and reduce the cell numbers in S phase of cell cycle. Increase of autophagosome in MG63 cytoplasm was observed under l uorescence microscope. Conclusions: Up-regulating the autophagy signii cantly reduced the sensitivity of MG63 cell to chemotherapy with DDP. DDP induced autophagy of MG63 cell and blocked the cell cycle at G1 phase. | Xu-Dong Miao Le Cao Qiang Zhang Xiao-Ying Hu Yi Zhang | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，9： | 3 |
| 20 | Clinical significance of microRNA-130b in osteosarcoma and its role in cell growth and invasion显示文摘Objective: To investigate clinical signii cance of microRNA-130b(mi R-130b) in osteosarcoma and its role in cell growth and invasion. Methods: miR-130b expression was detected in 68 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues by q RT-PCR. The expression of miR-130b was altered by corresponding vectors in osteosarcoma cells, and then Western blot was used to detect the expression of PPAR毭. Brd U cell proliferation and Transwell assays were performed to determine cell proliferation and invasion. Results: The expression of miR-130b in osteosarcoma tissues was signii cantly higher than that in normal tumor-adjacent tissues. Its expression in patients with metastasis was signii cantly higher than that in those without metastases. miR-130b expression in tumor tissues was signii cantly associated with tumor size, clinical stage and distant metastasis. And its expression was signii cantly correlated with overall survival and disease free survival. miR-130b overexpression obviously repressed the expression of PPAR毭, and resulted in signii cant increase of Saos-2 cell proliferation and invasion. On the contrast, repressing miR-130b expression with its inhibitor signii cantly increased PPAR毭 expression, and inhibited MG-63 cell proliferation and invasion. Conclusions: The high-expression of miR-130b is correlated with the adverse clinicopathological features and poor prognosis in osteosarcoma. miR-130b may regulate proliferation and invasion of osteosarcoma cells by targeting PPAR毭, suggesting miR-130b may play a key role in the progression of osteosarcoma. | Lie-Dao Yu Ri-Long Jin Peng-Cheng Gu Zhi-Heng Ling Xiang-Jin Lin Jing-Yu Du | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，9： | 3 |
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