The Experts below are selected from a list of 91851 Experts worldwide ranked by ideXlab platform
Xu Zhang - One of the best experts on this subject based on the ideXlab platform.
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circular rna ctfrc acts as the sponge of microRNA 107 to promote bladder carcinoma progression
Molecular Cancer, 2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression.
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Circular RNA cTFRC acts as the sponge of microRNA-107 to promote bladder carcinoma progression
BMC, 2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Abstract Background Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Methods Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. Results We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. Conclusions cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression
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Additional file 1: of Circular RNA cTFRC acts as the sponge of microRNA-107 to promote bladder carcinoma progression
2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Figure S1. TFRC expression is up-regulated and positively associated with advanced tumor grade of patients with BC. (A, B) TFRC mRNA expression in BC and their adjacent tissues, the data were obtained from TCGA BC data set (nonparametric Mann–Whitney test, **P
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microRNA 107 functions as a candidate tumor suppressor gene in renal clear cell carcinoma involving multiple genes
Urologic Oncology-seminars and Original Investigations, 2015Co-Authors: Nan Song, Yu Zhang, Xiaoxiong Wang, Pingkun Zhou, Xu ZhangAbstract:Abstract Background microRNAs (miRNAs) are small RNAs with oncogenic and tumor-suppressing functions in cancer. miRNAs not only regulate various target genes but also participate in vital signaling pathways. Methods and results The tumor-suppressing function of miRNA-107 (miR-107) was confirmed in clear cell renal cell carcinoma in 52 paired clinical specimens and renal cell carcinoma cell lines. Significant correlations were noted between clinical features and miR-107 expression level. Lentiviral vector and biosynthesis mimics were used to overexpress pre-miR-107 or mimicked miR-107 to investigate further the tumorigenesis of miR-107 in vivo and in vitro. Cell proliferation and invasiveness were inhibited in the 786-O cell line after miR-107 was delivered. High miR-107 level expression can apparently induce cell cycle arrest at the G2/M phase and retard tumor growth in nude mice. In addition, eukaryotic translation initiation factor 5 was found to be a direct target of miR-107 and exhibited an inverse relationship with miR-107. It was seen that p53 and VHL genes, which are implicated in renal tumors, were associated with miR-107. Conclusion In summary, our results showed that miR-107 can inhibit cell proliferation and invasiveness of renal cell carcinoma. Furthermore, this study may provide a potential therapeutic regimen for clear cell renal cell carcinoma treatment.
Tao Tao - One of the best experts on this subject based on the ideXlab platform.
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circular rna ctfrc acts as the sponge of microRNA 107 to promote bladder carcinoma progression
Molecular Cancer, 2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression.
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Circular RNA cTFRC acts as the sponge of microRNA-107 to promote bladder carcinoma progression
BMC, 2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Abstract Background Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Methods Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. Results We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. Conclusions cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression
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Additional file 1: of Circular RNA cTFRC acts as the sponge of microRNA-107 to promote bladder carcinoma progression
2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Figure S1. TFRC expression is up-regulated and positively associated with advanced tumor grade of patients with BC. (A, B) TFRC mRNA expression in BC and their adjacent tissues, the data were obtained from TCGA BC data set (nonparametric Mann–Whitney test, **P
Danyue Kang - One of the best experts on this subject based on the ideXlab platform.
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circular rna ctfrc acts as the sponge of microRNA 107 to promote bladder carcinoma progression
Molecular Cancer, 2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression.
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Circular RNA cTFRC acts as the sponge of microRNA-107 to promote bladder carcinoma progression
BMC, 2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Abstract Background Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Methods Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. Results We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. Conclusions cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression
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Additional file 1: of Circular RNA cTFRC acts as the sponge of microRNA-107 to promote bladder carcinoma progression
2019Co-Authors: Tao Tao, Zhao Yang, Xing Kang, Xu Zhang, Danyue KangAbstract:Figure S1. TFRC expression is up-regulated and positively associated with advanced tumor grade of patients with BC. (A, B) TFRC mRNA expression in BC and their adjacent tissues, the data were obtained from TCGA BC data set (nonparametric Mann–Whitney test, **P
Quintin Pan - One of the best experts on this subject based on the ideXlab platform.
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microRNA 107 functions as a candidate tumor suppressor gene in head and neck squamous cell carcinoma by downregulation of protein kinase cɛ
Oncogene, 2012Co-Authors: Jharna Datta, Ashley Smith, James C Lang, Mozaffarul Islam, Debleena Dutt, Theodoros N Teknos, Quintin PanAbstract:Head and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent cancer worldwide with about 600 000 new cases diagnosed each year. Understanding the molecular pathways that lead to HNSCC is crucial to identify new targets for anti-cancer drug development. Protein kinase Cɛ (PKCɛ) is elevated in HNSCC and regulates the activation of Akt, Stat3 and Rho GTPases. To date, the molecular mechanism of PKCɛ dysregulation in HNSCC remains to be elucidated. In silico analysis identified three putative microRNA-107 (miR-107) binding sites in the 3′-untranslated region (UTR) of PKCɛ. An inverse relationship was revealed between miR-107 and PKCɛ in HNSCC cell lines. Delivery of miR-107 reduced PKCɛ levels in SCC15, SCC25 and CAL27, three HNSCC cell lines with high PKCɛ and low miR-107. The activity of a luciferase reporter construct containing the 3′-UTR of PKCɛ was downregulated by miR-107 and mutations in the three cognate miR-107 binding sites completely ablated the regulation by miR-107. Treatment with miR-107 significantly blocked cell proliferation, DNA replication, colony formation and invasion in SCC25 and CAL27 cells. Ectopic expression of miR-resistant PKCɛ was sufficient to partially rescue the loss-of-function phenotype in miR-107-overexpressing SCC25 cells. Tumor growth in nude mice was retarded by 93±7% in CAL27/miR-107 cells compared with CAL27/miR-control cells. Last, human primary HNSCC tumors with elevated PKCɛ had reduced miR-107 expression. Our results demonstrate that PKCɛ is directly regulated by miR-107 and, moreover, suggest that miR-107 may be a potential anti-cancer therapeutic for HNSCC.
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abstract 1153 nanoparticle delivery of microRNA 107 reduces the tumorigenicity of head and neck squamous carcinoma hnscc
Cancer Research, 2011Co-Authors: Longzhu Piao, Theodoros N Teknos, Manchao Zhang, Sanjay L Bhave, Quintin PanAbstract:Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL Head and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent cancer worldwide with about 600,000 new cases diagnosed in the last year. The 5-year survival rate of HNSCC has remained stagnant despite advances in the clinical management of this disease. Understanding the molecular pathways that lead to aggressive HNSCC is crucial to identify new “druggable” targets for anti-cancer drug development. Recently, our laboratory showed that miR-107 is significantly reduced in primary HNSCC tumors and HNSCC cell lines. Ectopic expression of miR-107 in CAL-27 HNSCC cells significantly inhibited cell proliferation, DNA replication, clonogenic survival, and tumor growth in nude mice. Our data demonstrate the potential application of miR-107 as a novel anti-cancer therapeutic for HNSCC. In this study, we determine the efficacy of miR-107 encapsulated nanoparticles (NP-miR-107) in a xenograft model of HNSCC. NP-miR-107 was successfully formulated by ethanol injection method. The particle size of NP-miR-107 was 47.8 ± 3.5 nm and zeta potential was +12.1 mV. NP-miR-107 significantly retarded (57.6% inhibition, p<0.02) tumor growth of CAL27 HNSCC tumors compared to NP-miR-control; tumor volume of 340.6 ± 51.6 mm3 and 804.1 ± 181.6 mm3 for the NP-miR-107 group and the NP-miR-control group, respectively. Moreover, Kaplan-Meir analysis showed a survival advantage for the NP-miR-107 treatment group (p=0.039). Our results demonstrate that our nanoparticles are an effective carrier approach to deliver therapeutic miRs to tumors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1153. doi:10.1158/1538-7445.AM2011-1153
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abstract 144 microRNA 107 regulates pkcepsilon and functions as a tumor suppressor mir in head and neck squamous cell carcinoma
Cancer Research, 2011Co-Authors: Jharna Datta, Ashley Smith, James C Lang, Mozaffarul Islam, Theodoros N Teknos, Quintin PanAbstract:Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL Head and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent cancer worldwide with about 600,000 new cases diagnosed in the last year. The 5-year survival rate of HNSCC has remained stagnant despite advances in the clinical management of this disease. Understanding the molecular pathways that lead to aggressive HNSCC is crucial to identify new “druggable” targets for anti-cancer drug development. Protein kinase Cepsilon (PKCe) is elevated in HNSCC and regulates cell invasion and motility thorough activation of Rho GTPases. Our laboratory and others provide evidence that PKCe is a transforming oncogene that phosphorylates and modulates a cascade of signal transduction pathways, including Akt, EGFR, Rho GTPases, and Stat3. Thus, targeting PKCe may be an attractive therapeutic approach to dampen multiple hyper-active signaling pathways in concert. At this time, the molecular mechanism of PKCe dysregulation in HNSCC remains to be elucidated. In silico analysis with TargetScan, MiRBase, and miRanda identified numerous putative microRNA (miR) binding sites in the 3’-UTR region of PKCe. We screened a panel of miRs using qPCR and miR-107 was identified to have an inverse association with PKCe in HNSCC cell lines with high endogenous PKCe. Ectopic expression of miR-107 in several HNSCC cell lines significantly reduced PKCe mRNA expression and protein levels. The expression of a luciferase reporter construct containing the 3’-UTR of PKCe was down-regulated by miR-107 and deletion/mutation of the three cognate miR-107 binding sites completely abolished the regulation by miR-107. These observations confirm PKCe as a validated target of miR-107. Ectopic expression of miR-107 in HNSCC cell lines significantly inhibited cell proliferation, DNA replication, clonogenic survival, invasion and migration. Tumor take and tumor growth of HNSCC cells was suppressed by miR-107 in a pre-clinical nude mouse model of HNSCC. Lastly, miR-107 was significantly reduced and showed an inverse expression relationship with PKCe in human primary HNSCC tumors. These results indicate that miR-107 regulates PKCe levels to control the tumorigenicity of HNSCC cells. Taken together, our data substantiate the potential application of miR-107 as a novel anti-cancer therapeutic for HNSCC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 144. doi:10.1158/1538-7445.AM2011-144
Xiao-dan Jiang - One of the best experts on this subject based on the ideXlab platform.
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microRNA 107 inhibits u87 glioma stem cells growth and invasion
Cellular and Molecular Neurobiology, 2013Co-Authors: Lei Chen, Run Zhang, Yi Liu, Xiangrong Chen, Fanfan Chen, Ke Yan, Xiao-dan JiangAbstract:Glioma stem cells (GSCs) are thought to be critical for resistance to radiotherapy and chemotherapy and for tumor recurrence after surgery in glioma patients. Identification of new therapeutic strategies that can target GSCs may thus be critical for improving patient survival. microRNAs (miRNAs) are small non-coding RNAs that function as tumor suppressors or oncogenes. In this study, we confirmed that miR-107 was down-regulated in GSCs. To investigate the role of miR-107 in tumorigenesis of GSCs, a lentiviral vector over-expressing miR-107 in U87GSCs was constructed. We found that over-expression of miR-107 suppressed proliferation and down-regulated Notch2 protein and stem cell marker (CD133 and Nestin) expression in U87GSCs. Furthermore, enhanced miR-107 expression significantly inhibited U87GSC invasion and reduced matrix metalloproteinase-12 expression. miR-107 also suppressed U87GSCs xenograft growth in vivo. These findings suggest that miR-107 is involved in U87GSCs growth and invasion and may provide a potential therapeutic target for glioma treatment.
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microRNA 107 inhibits glioma cell migration and invasion by modulating notch2 expression
Journal of Neuro-oncology, 2013Co-Authors: Lei Chen, Run Zhang, Yi Liu, Xiangrong Chen, Ke Yan, Xiao-dan JiangAbstract:microRNAs (miRNAs), small non-protein-coding RNA molecules, modulate target gene expression by binding to 3'untranslated regions (UTR) of target mRNA. These molecules are aberrantly expressed in many human cancers, and can function either as tumor suppressors or oncogenes. In the current study, we show that miR-107 is down-regulated in glioma tissues and cell lines, and its overexpression leads to inhibition of the migratory and invasive ability of glioma cells via direct targeting of Notch2, which is known to transactivate Tenascin-C and Cox-2. Experiments with Notch2 siRNA further suggest that miR-107 may exerts its anti-invasive activity through Notch2 signaling pathways. Our findings collectively indicate that miR-107 is involved in glioma cell migration and invasion, and support its utility as a potential target for glioma treatment.
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P53-induced microRNA-107 inhibits proliferation of glioma cells and down-regulates the expression of CDK6 and Notch-2.
Neuroscience letters, 2012Co-Authors: Lei Chen, Run Zhang, Yi Liu, Kun Qin, Yi-jing Liu, Xiao-dan JiangAbstract:Abstract microRNAs (miRNAs) are small noncoding RNAs that function as tumor suppressors or oncogenes. microRNA-107 (miR-107), a transcriptional target of p53, is deregulated in many cancer cell lines. Here, we showed that miR-107 is down-regulated in glioma tissues and cell lines, in particular, p53-mutated U251 and A172. Transfection of wild-type p53 into these cells stimulated miR-107 expression. To investigate the role of miR-107 in tumorigenesis, we constructed a lentiviral vector overexpressing miR-107. Notably, miR-107 inhibited proliferation and arrested the cell cycle at the G0–G1 phase in glioma cells. Transduction of Lenti-GFP-miR-107 into glioma cells inhibited CDK6 and Notch-2 protein expression. Our findings collectively demonstrate that p53-induced miR-107 suppresses brain tumor cell growth and down-regulates CDK6 and Notch-2 expression, supporting its tumor suppressor role and utility as a target for glioma therapy.