The Experts below are selected from a list of 3480 Experts worldwide ranked by ideXlab platform

Liang Yang - One of the best experts on this subject based on the ideXlab platform.

  • Long non-coding RNA HOTAIR promotes exosome secretion by regulating RAB35 and SNAP23 in hepatocellular carcinoma
    Molecular Cancer, 2019
    Co-Authors: Liang Yang, Yingbo Ma, Chunli Wu, Xueqiang Peng, Yan Li, Xiaodong Zhang, Hangyu Li
    Abstract:

    Emerging evidence indicates that tumor cells release a large amount of exosomes loaded with cargos during tumorigenesis. Exosome secretion is a multi-step process regulated by certain related molecules. Long non-coding RNAs (lncRNAs) play an important role in hepatocellular carcinoma (HCC) progression. However, the role of lncRNA HOTAIR in regulating exosome secretion in HCC cells remains unclear. We analyzed the relationship between HOTAIR expression and exosome secretion-related genes using gene set enrichment analysis (GSEA). Nanoparticle tracking analysis was performed to validate the effect of HOTAIR on exosome secretion. The transport of multivesicular bodies (MVBs) after overexpression of HOTAIR was detected by transmission electron microscopy and confocal microscopy analysis of cluster determinant 63 (CD63) with synaptosome associated protein 23 (SNAP23). The mechanism of HOTAIR’s regulation of Ras-related protein Rab-35 (RAB35), vesicle associated membrane protein 3 (VAMP3), and SNAP23 was assessed using confocal co-localization analysis, phosphorylation assays, and rescue experiments. We found an enrichment of exosome secretion-related genes in the HOTAIR high expression group. HOTAIR promoted the release of exosomes by inducing MVB transport to the plasma membrane. HOTAIR regulated RAB35 expression and localization, which controlled the docking process. Moreover, HOTAIR facilitated the final step of fusion by influencing VAMP3 and SNAP23 colocalization. In addition, we validated that HOTAIR induced the phosphorylation of SNAP23 via mammalian target of rapamycin (mTOR) signaling. Our study demonstrated a novel function of lncRNA HOTAIR in promoting exosome secretion from HCC cells and provided a new understanding of lncRNAs in tumor cell biology.

  • Long non-coding RNA HOTAIR promotes exosome secretion by regulating RAB35 and SNAP23 in hepatocellular carcinoma
    BMC, 2019
    Co-Authors: Liang Yang, Xueqiang Peng, Xiaodong Zhang, Shibo Wei, Qing Fan, Jingang Liu
    Abstract:

    Abstract Background Emerging evidence indicates that tumor cells release a large amount of exosomes loaded with cargos during tumorigenesis. Exosome secretion is a multi-step process regulated by certain related molecules. Long non-coding RNAs (lncRNAs) play an important role in hepatocellular carcinoma (HCC) progression. However, the role of lncRNA HOTAIR in regulating exosome secretion in HCC cells remains unclear. Methods We analyzed the relationship between HOTAIR expression and exosome secretion-related genes using gene set enrichment analysis (GSEA). Nanoparticle tracking analysis was performed to validate the effect of HOTAIR on exosome secretion. The transport of multivesicular bodies (MVBs) after overexpression of HOTAIR was detected by transmission electron microscopy and confocal microscopy analysis of cluster determinant 63 (CD63) with synaptosome associated protein 23 (SNAP23). The mechanism of HOTAIR’s regulation of Ras-related protein Rab-35 (RAB35), vesicle associated membrane protein 3 (VAMP3), and SNAP23 was assessed using confocal co-localization analysis, phosphorylation assays, and rescue experiments. Results We found an enrichment of exosome secretion-related genes in the HOTAIR high expression group. HOTAIR promoted the release of exosomes by inducing MVB transport to the plasma membrane. HOTAIR regulated RAB35 expression and localization, which controlled the docking process. Moreover, HOTAIR facilitated the final step of fusion by influencing VAMP3 and SNAP23 colocalization. In addition, we validated that HOTAIR induced the phosphorylation of SNAP23 via mammalian target of rapamycin (mTOR) signaling. Conclusion Our study demonstrated a novel function of lncRNA HOTAIR in promoting exosome secretion from HCC cells and provided a new understanding of lncRNAs in tumor cell biology

  • Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling
    Oncology reports, 2017
    Co-Authors: Shibo Wei, Liang Yang, Xiaodong Zhang, Qing Fan, Zhi-hong Zong, Xiangdong Hua, Hongzhi Sun
    Abstract:

    Abstract The long non-coding RNA HOX transcript antisense RNA (HOTAIR) plays a key role in the progression of various carcinomas. However, whether or not HOTAIR influences glucose metabolism and the specific underlying mechanism in hepatocellular carcinoma (HCC) cells remain unclear. In the present study, we found markedly increased HOTAIR expression in 84 HCC tissues and demonstrated that HOTAIR overexpression promoted cell proliferation using Cell Counting Kit-8. The effect on glucose metabolism regulated by HOTAIR in HCC cells was determined by detecting lactate and glucose levels: HOTAIR promoted glycolysis by upregulating glucose transporter isoform 1 (GLUT1) and activating mammalian target of rapamycin (mTOR) signaling, whereas knockdown of HOTAIR suppressed this effect. Our research reveals a novel relationship between HOTAIR and glucose metabolism in HCC cells, and it may be a therapeutic target for diagnosing and treating HCC.

  • the long noncoding rna HOTAIR activates autophagy by upregulating atg3 and atg7 in hepatocellular carcinoma
    Molecular BioSystems, 2016
    Co-Authors: Liang Yang, Xiuwei Zhang, Jingang Liu
    Abstract:

    The long noncoding RNA HOX transcript antisense RNA (HOTAIR) has been reported to be an oncogene that influences tumor cell development and that correlates with prognosis in hepatocellular carcinoma (HCC). Accumulating evidence indicates that autophagy plays a significant role in tumorigenesis and cancer cell survival, but whether HOTAIR modulates autophagy in HCC cells remains unknown. In this study, HOTAIR expression was measured in 54 matched paired HCC tissues and the adjacent non-tumor tissues. HOTAIR was overexpressed in the HCC tissues as compared with the adjacent non-tumor tissues and was associated with tumor size. In vitro assays revealed that the overexpression of HOTAIR promoted the activation of autophagy in HCC cell lines, whereas HOTAIR knockdown suppressed it. Further investigation revealed that overexpressed HOTAIR upregulated autophagy-related 3 (ATG3) and ATG7 expression in HCC cells. In conclusion, HOTAIR, overexpressed in HCC and associated with tumor size, could activate autophagy by increasing ATG3 and ATG7 expression, promoting HCC cell proliferation.

Te Liu - One of the best experts on this subject based on the ideXlab platform.

  • suppressed expression of long non coding rna HOTAIR inhibits proliferation and tumourigenicity of renal carcinoma cells
    Tumor Biology, 2014
    Co-Authors: Junfeng Liu, Yin Zheng, Li You, Dingwei Kuang, Te Liu
    Abstract:

    Although long non-coding RNAs (lncRNAs) are known to play an important role in cell regulation in several cancers, the regulatory mechanisms in renal carcinoma cells remain unclear. HOX transcript antisense RNA (HOTAIR), an lncRNA, coordinates with chromatin-modifying enzymes to regulate gene silencing. HOTAIR is over-expressed in several types of carcinoma cells. Thus, we hypothesised that lncRNA HOTAIR is crucial for cell proliferation and invasion and that its knockdown induces apoptosis in renal carcinoma cells. lncRNA HOTAIR expression was found to be elevated in renal carcinoma cells. Additionally, lncRNA HOTAIR knockdown by RNA interference with siRNA was found to significantly affect the cell cycle in the G0/G1 phase and weaken the abilities of cell proliferation and invasion in vitro. Xenograft experiments confirmed that the growth of xenograft tumours formed by renal carcinoma cells was suppressed after silencing lncRNA HOTAIR expression. Moreover, chromatin immunoprecipitation (ChIP) and RNA-binding protein immunoprecipitation (RIP) assays revealed that knockdown of lncRNA HOTAIR led to the weakening of the recruitment and binding abilities of EZH2 and H3K27me3 locus with lncRNA HOTAIR. Furthermore, the cell cycle-related gene locus was in an active transcriptional state by the silencing of lncRNA HOTAIR expression and modulation of covalent histones.

Hangyu Li - One of the best experts on this subject based on the ideXlab platform.

  • Long non-coding RNA HOTAIR promotes exosome secretion by regulating RAB35 and SNAP23 in hepatocellular carcinoma
    Molecular Cancer, 2019
    Co-Authors: Liang Yang, Yingbo Ma, Chunli Wu, Xueqiang Peng, Yan Li, Xiaodong Zhang, Hangyu Li
    Abstract:

    Emerging evidence indicates that tumor cells release a large amount of exosomes loaded with cargos during tumorigenesis. Exosome secretion is a multi-step process regulated by certain related molecules. Long non-coding RNAs (lncRNAs) play an important role in hepatocellular carcinoma (HCC) progression. However, the role of lncRNA HOTAIR in regulating exosome secretion in HCC cells remains unclear. We analyzed the relationship between HOTAIR expression and exosome secretion-related genes using gene set enrichment analysis (GSEA). Nanoparticle tracking analysis was performed to validate the effect of HOTAIR on exosome secretion. The transport of multivesicular bodies (MVBs) after overexpression of HOTAIR was detected by transmission electron microscopy and confocal microscopy analysis of cluster determinant 63 (CD63) with synaptosome associated protein 23 (SNAP23). The mechanism of HOTAIR’s regulation of Ras-related protein Rab-35 (RAB35), vesicle associated membrane protein 3 (VAMP3), and SNAP23 was assessed using confocal co-localization analysis, phosphorylation assays, and rescue experiments. We found an enrichment of exosome secretion-related genes in the HOTAIR high expression group. HOTAIR promoted the release of exosomes by inducing MVB transport to the plasma membrane. HOTAIR regulated RAB35 expression and localization, which controlled the docking process. Moreover, HOTAIR facilitated the final step of fusion by influencing VAMP3 and SNAP23 colocalization. In addition, we validated that HOTAIR induced the phosphorylation of SNAP23 via mammalian target of rapamycin (mTOR) signaling. Our study demonstrated a novel function of lncRNA HOTAIR in promoting exosome secretion from HCC cells and provided a new understanding of lncRNAs in tumor cell biology.

Xiaodong Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Long non-coding RNA HOTAIR promotes exosome secretion by regulating RAB35 and SNAP23 in hepatocellular carcinoma
    Molecular Cancer, 2019
    Co-Authors: Liang Yang, Yingbo Ma, Chunli Wu, Xueqiang Peng, Yan Li, Xiaodong Zhang, Hangyu Li
    Abstract:

    Emerging evidence indicates that tumor cells release a large amount of exosomes loaded with cargos during tumorigenesis. Exosome secretion is a multi-step process regulated by certain related molecules. Long non-coding RNAs (lncRNAs) play an important role in hepatocellular carcinoma (HCC) progression. However, the role of lncRNA HOTAIR in regulating exosome secretion in HCC cells remains unclear. We analyzed the relationship between HOTAIR expression and exosome secretion-related genes using gene set enrichment analysis (GSEA). Nanoparticle tracking analysis was performed to validate the effect of HOTAIR on exosome secretion. The transport of multivesicular bodies (MVBs) after overexpression of HOTAIR was detected by transmission electron microscopy and confocal microscopy analysis of cluster determinant 63 (CD63) with synaptosome associated protein 23 (SNAP23). The mechanism of HOTAIR’s regulation of Ras-related protein Rab-35 (RAB35), vesicle associated membrane protein 3 (VAMP3), and SNAP23 was assessed using confocal co-localization analysis, phosphorylation assays, and rescue experiments. We found an enrichment of exosome secretion-related genes in the HOTAIR high expression group. HOTAIR promoted the release of exosomes by inducing MVB transport to the plasma membrane. HOTAIR regulated RAB35 expression and localization, which controlled the docking process. Moreover, HOTAIR facilitated the final step of fusion by influencing VAMP3 and SNAP23 colocalization. In addition, we validated that HOTAIR induced the phosphorylation of SNAP23 via mammalian target of rapamycin (mTOR) signaling. Our study demonstrated a novel function of lncRNA HOTAIR in promoting exosome secretion from HCC cells and provided a new understanding of lncRNAs in tumor cell biology.

  • Long non-coding RNA HOTAIR promotes exosome secretion by regulating RAB35 and SNAP23 in hepatocellular carcinoma
    BMC, 2019
    Co-Authors: Liang Yang, Xueqiang Peng, Xiaodong Zhang, Shibo Wei, Qing Fan, Jingang Liu
    Abstract:

    Abstract Background Emerging evidence indicates that tumor cells release a large amount of exosomes loaded with cargos during tumorigenesis. Exosome secretion is a multi-step process regulated by certain related molecules. Long non-coding RNAs (lncRNAs) play an important role in hepatocellular carcinoma (HCC) progression. However, the role of lncRNA HOTAIR in regulating exosome secretion in HCC cells remains unclear. Methods We analyzed the relationship between HOTAIR expression and exosome secretion-related genes using gene set enrichment analysis (GSEA). Nanoparticle tracking analysis was performed to validate the effect of HOTAIR on exosome secretion. The transport of multivesicular bodies (MVBs) after overexpression of HOTAIR was detected by transmission electron microscopy and confocal microscopy analysis of cluster determinant 63 (CD63) with synaptosome associated protein 23 (SNAP23). The mechanism of HOTAIR’s regulation of Ras-related protein Rab-35 (RAB35), vesicle associated membrane protein 3 (VAMP3), and SNAP23 was assessed using confocal co-localization analysis, phosphorylation assays, and rescue experiments. Results We found an enrichment of exosome secretion-related genes in the HOTAIR high expression group. HOTAIR promoted the release of exosomes by inducing MVB transport to the plasma membrane. HOTAIR regulated RAB35 expression and localization, which controlled the docking process. Moreover, HOTAIR facilitated the final step of fusion by influencing VAMP3 and SNAP23 colocalization. In addition, we validated that HOTAIR induced the phosphorylation of SNAP23 via mammalian target of rapamycin (mTOR) signaling. Conclusion Our study demonstrated a novel function of lncRNA HOTAIR in promoting exosome secretion from HCC cells and provided a new understanding of lncRNAs in tumor cell biology

  • Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling
    Oncology reports, 2017
    Co-Authors: Shibo Wei, Liang Yang, Xiaodong Zhang, Qing Fan, Zhi-hong Zong, Xiangdong Hua, Hongzhi Sun
    Abstract:

    Abstract The long non-coding RNA HOX transcript antisense RNA (HOTAIR) plays a key role in the progression of various carcinomas. However, whether or not HOTAIR influences glucose metabolism and the specific underlying mechanism in hepatocellular carcinoma (HCC) cells remain unclear. In the present study, we found markedly increased HOTAIR expression in 84 HCC tissues and demonstrated that HOTAIR overexpression promoted cell proliferation using Cell Counting Kit-8. The effect on glucose metabolism regulated by HOTAIR in HCC cells was determined by detecting lactate and glucose levels: HOTAIR promoted glycolysis by upregulating glucose transporter isoform 1 (GLUT1) and activating mammalian target of rapamycin (mTOR) signaling, whereas knockdown of HOTAIR suppressed this effect. Our research reveals a novel relationship between HOTAIR and glucose metabolism in HCC cells, and it may be a therapeutic target for diagnosing and treating HCC.

Chongyun Xing - One of the best experts on this subject based on the ideXlab platform.

  • Long noncoding RNA HOTAIR promotes the self-renewal of leukemia stem cells through epigenetic silencing of p15.
    Experimental hematology, 2018
    Co-Authors: Shenmeng Gao, Bin Zhou, Xingzhou Huang, Chongyun Xing
    Abstract:

    Acute myeloid leukemia (AML) is a heterogeneous hematopoietic disorder initiated from a small subset of leukemia stem cell (LSC), which presents unrestricted self-renewal and proliferation. Long non-coding RNA HOTAIR is abundantly expressed and plays oncogenic roles in solid cancer and AML. However, whether HOTAIR regulates the self-renewal of LSC is largely unknown. Here, we reported that the expression of HOTAIR was increased in LSC than in normal hematological stem and progenitor cells (HSPCs). HOTAIR inhibition by short hairpin RNAs (shRNAs) decreased colony formation in leukemia cell lines and primary AML blasts. We then investigated the role of HOTAIR in leukemia in vivo. HOTAIR knockdown extends the survival time in U937-transplanted NSG mice. Furthermore, HOTAIR knockdown reduced infiltration of leukemic blasts, decreased frequency of LSC, and prolonged overall survival in MLL-AF9-induced murine leukemia, suggesting that HOTAIR is required for the maintenance of AML. Mechanistically, HOTAIR inhibited p15 expression through zeste homolog 2 (EZH2)-enrolled tri-methylation of Lys 27 of histone H3 (H3K27me3) in p15 promoter. In addition, p15 partially reversed the decrease of colony and proliferation induced by HOTAIR knockdown, suggesting that p15 plays an important role in the leukemogenesis by HOTAIR. In conclusion, our study suggests that HOTAIR facilitates leukemogenesis by enhancing self-renewal of LSC. HOTAIR might be a potential target for anti-LSC therapy.

  • long non coding rna HOTAIR modulates c kit expression through sponging mir 193a in acute myeloid leukemia
    FEBS Letters, 2015
    Co-Authors: Chongyun Xing, Feiyan Xie, Liyuan Tang, Shenmeng Gao
    Abstract:

    HOTAIR is significantly overexpressed in various cancers and facilitates tumor invasion and metastasis. However, whether HOTAIR plays oncogenic roles in acute myeloid leukemia (AML) is still unknown. Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Clinically, AML patients with higher HOTAIR predicted worse clinical outcome compared with those with lower HOTAIR. Importantly, HOTAIR knockdown by small hairpin RNA inhibited cell growth, induced apoptosis, and decreased number of colony formation. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.