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• Research Paper Volume 11, Issue 15 pp 5351-5367

  Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom

  Relevance score: 6.401277

  Wen Guo, Qing Yu, Ming Zhang, Fang Li, Yu Liu, Weiwei Jiang, Haitao Jiang, Haijun Li

  Keywords: osteosarcoma, LINC00511, miR-618, MAEL, aging, age-related diseases

  Published in Aging on August 6, 2019

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  Osteosarcoma is a tumor disease that commonly exists among young populations. Our research explored the role of the LINC00511/microRNA-618/MAEL axis in osteosarcoma.

  Expression profiles of long non-coding RNAs (lncRNAs) in osteosarcoma (OS) tissues were constructed, and LINC00511 expression levels were verified with qRT-PCR. LncRNA-miRNA and miRNA-mRNA interactions were predicted. Validation was performed using a dual-luciferase reporter assay. Protein expression levels of MAEL were evaluated by Western blot assays. The effects of LINC00511, miR-618 and MAEL on the proliferation, viability, and metastasis of OS cells were detected using colony formation, cell counting kit-8 (CCK-8) and transwell assays, respectively. The apoptosis rates of OS cells were investigated using flow cytometry. The tumor-suppressing effect of LINC00511 silencing was also analyzed using a xenograft model in nude mice.

  LINC00511 overexpression was observed in OS tissues and cell lines. Knockdown of LINC00511 in nude mice inhibited the tumorigenic ability of OS cells. Transfection-induced overexpression of LINC00511 and MAEL, as well as downregulation, highlighted the features of tumor cells, and LINC00511 overexpression reduced apoptosis in vitro.

  LINC00511 was confirmed to be beneficial for osteosarcoma development via sponging miR-618 and increasing MAEL expression and may thus be considered a potential target for osteosarcoma therapy.

  

  LncRNA microarray analysis and high expression of LINC00511 in OS. (A) Heatmap of lncRNA expression in OS tissues (n=6). LncRNAs were selected based on Flod change value>2 and P<0.05; the overexpressed lncRNAs are shown in red, and the downregulated lncRNAs are shown in green. (B) The expression of LINC00511 in Tumor tissues was higher than that in adjacent tissues as detected by qRT-PCR. **P<0.01 compared to the Adjacent group. (C) The expression of LINC00511 in OS cell lines, including MG-63, HOS, Saos-2 and 143B. *P<0.05 and **P<0.01 compared to the noncancerous osteoblast cell line hFOB 1.19.

  
  
  

  

  LINC00511 mediates the cell proliferation and apoptosis of HOS cells in vitro. (A) The relative expression level of LINC00511 was changed in HOS cells transfected with p-LINC00511- or LINC00511-targeting siRNA. P-LINC00511 is a LINC00511 overexpression vector, and its transfection induced a high level of LINC00511 expression. In contrast, transfection of specific LINC00511-targeting siRNA caused low expression levels of LINC00511 in HOS cells. (B) CCK-8 assays showed that the proliferation ability is changed in HOS cells with LINC00511 dysregulation. Up- or downregulation of LINC00511 was induced by pre-transfection with p-LINC00511 or specific siRNA. (C–D) Colony formation ability of HOS cells with altered expression of LINC00511. (E–F) Apoptosis rate of HOS cells with altered expression of LINC00511. *P < 0.05 compared to the NC group.

  
  
  

  

  In vitro migration and invasion activities of HOS cells with LINC00511 dysregulation. (A, C) In vitro migration ability of HOS cells with dysregulation of LINC00511. (B, D) In vitro invasion ability of HOS cells with dysregulation of LINC00511. Both migration and invasion abilities were detected using a transwell assay. LINC00511 dysregulation in HOS cells was induced by the pre-transfection of p-LINC00511 (upregulation) or specific siRNA (downregulation). *P < 0.05 compared to the NC group.

  
  
  

  

  LINC00511 promotes the tumorigenesis of OS in nude mice. (A) Xenografts formed by HOS cells with normal (upper) or downregulated (bottom) expression of LINC00511. Tumor tissues were harvested after 3 weeks of implantation (Scale bar, 0.5 cm). (B) Expression level of LINC00511 in the xenografts tissues. *P<0.05 compared with NC group. (C–D) SiRNA-induced downregulation of LINC00511 inhibited the growth of xenografts in nude mice. The volumes of xenografts were measured every 3 days, and their weights were measured after harvesting. (E) Xenografts formed by HOS cells with normal (upper) or downregulated (bottom) expression of LINC00511. Tumor tissues were harvested after 3 weeks of implantation (Scale bar, 0.5 cm). Lenti-sh-LINC00511 cells were transfected with lentivirus-mediated shRNA targeting LINC00511. Lenti-sh-ctrl means cells were transfected with shRNA lentiviral particles with nontargeting scrambled shRNA sequences. (F) The LINC00511 expression level in lenti-sh-LINC00511 group was markedly decreased compared to that in the lenti-sh-ctrl group. (G–H) ShRNA-induced downregulation of LINC00511 inhibited the growth of xenografts in nude mice. The volumes of xenografts were measured every 3 days, and their weights were measured after harvesting. *P<0.05 compared to the lenti-sh-ctrl group.

  
  
  

  

  LINC00511 suppressed the expression of miR-618 in HOS cells. (A) The target relationship between miR-618 and LINC00511 was predicted by bioinformatics analysis (upper) and validated by dual-luciferase reporter assays (bottom). MiR-618 mimics significantly inhibit the fluorescence activity of the reporter vector carrying wild-type LINC00511, but not mutant LINC00511. *P<0.05 compared with the NC group. (B) The expression of miR-618 in OS tissues and adjacent tissues was measured using qRT-PCR. *P<0.05 compared to the adjacent group. (C) Downregulated expression of miR-618 in OS cell lines detected by qRT-PCR analysis. *P<0.05 compared with the noncancerous osteoblast cell line hFOB 1.19. (D) Expression of miR-618 in HOS cells is inhibited by LINC00511. *P<0.05 compared to the NC group.

  
  
  

  

  MiR-618 inhibits the in vitro activity of OS cells. (A) Expression profiles of miR-618 in HOS cells transfected with miR-618 mimics (upregulation), miR-618 inhibitor (downregulation) or si-LINC00511+miR-618 inhibitor (not changed). (B–E) CCK-8, colony formation and transwell assays of the proliferation, migration and invasion ability of HOS cells with miR-618 dysregulation. (B) CCK-8 assay for cell viability. (C) Colony formation assay for cell proliferation. (D) Transwell assay for cell migration. (E) Transwell assay for cell invasion. *P<0.05 compared to the NC group.

  
  
  

  

  The expression of MAEL is mediated by both miR-618 and LINC00511. (A) Binding sites between miR-618 and MAEL were predicted by TargetScanHuman7.2. Then, the target relationship between miR-618 and MAEL was validated by a dual-luciferase reporter assay. MiR-618 mimics significantly inhibited the expression of luciferase reporter vectors carrying the wild-type MAEL sequence but not the mutated MAEL sequence. *P<0.05 compared to the NC group. (B) A qRT-PCR assay shows that MAEL mRNA expression was higher in OS tissues than in corresponding normal tissues. *P<0.05 compared to the adjacent group. (C–D) MAEL protein expression levels were detected in OS tissues and adjacent normal tissues by Western blot assay (N=10). (E–F) MAEL mRNA (E) and protein (F) expression levels in OS cell lines. *P<0.05 and **P<0.01 compared to the noncancerous osteoblast cell line hFOB 1.19. (G–H) MAEL mRNA (G) and protein (H) expression levels in HOS cells transfected with NC, p-LINC00511, siRNA-LINC00511, and miR-618 inhibitor or mimics were tested by qRT-PCR and Western blot assays. *P<0.05 compared to the NC group.

  
  
  

  

  MiR-618 promotes the tumor activity of OS cells in vitro. (A) Specific siRNA inhibited the expression of MAEL mRNA in HOS cells. (B) MAEL protein expression was dramatically lower in the si-MEAL group than in the NC group. (C–E) CCK-8, colony formation and transwell assays of the proliferation, migration and invasion abilities of HOS cells with MAEL silencing. (C) CCK-8 assay for cell viability. (D) Colony formation assay for cell proliferation. (E) Transwell assays for cell migration and invasion. *P<0.05 and **P<0.01 compared to the NC group.

  
  
  

• Research Paper pp undefined-undefined

  MAEL in human cancers and implications in prognostication and predicting benefit from immunotherapy over VEGFR/mTOR inhibitors in clear cell renal cell carcinoma: a bioinformatic analysis

  Relevance score: 6.365692

  Jin Tao, Jinshan Cui, Yu Xu, Yafeng Fan, Guodong Hong, Qiaoxia Zhou, Guoqiang Wang, Leo Li, Yusheng Han, Chunwei Xu, Wenxian Wang, Shangli Cai, Xuepei Zhang

  Keywords: MAEL, pan-cancer analysis, clear cell renal cell carcinoma, prognosis, immunotherapy

  Published in Aging on Invalid Date

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  Maelstrom (MAEL), a novel cancer/testis-associated gene, may facilitate the initiation and progression of human malignancies, warranting comprehensive investigations. Single-cell and tissue-bulk transcriptomic data demonstrated higher MAEL expression in testis (spermatogonia/spermatocyte), kidney (proximal tubular cell), and brain (neuron/astrocyte), and corresponding cancers, including testicular germ cell tumor, glioma, papillary renal cell carcinoma, and clear cell renal cell carcinoma (ccRCC). Of these cancers, only in ccRCC did MAEL expression exhibit associations with both recurrence-free survival and overall survival. High MAEL expression was associated with an anti-inflammatory tumor immune microenvironment and VEGFR/mTOR activation in ccRCC tissues and high sensitivities to VEGFR/PI3K-AKT-mTOR inhibitors in ccRCC cell lines. Consistent with these, low rather than high MAEL expression indicated remarkable progression-free survival benefits from immune checkpoint inhibitor (ICI)-based immunotherapies over VEGFR/mTOR inhibitors in two large phase III trials (JAVELIN Renal 101 and CheckMate-025). MAEL is a biologically and clinically significant determinant with potential for prognostication after nephrectomy and patient selection for VEGFR/mTOR inhibitors and immunotherapy-based treatments.