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  ✔本篇論文使用華聯產品:Human miRNA OneArray  
 Journal Of Cellular Biochemistry. 2014 Feb 12. doi: 10.1002/jcb.24786.
 Regulatory Roles of miRNA in the Human Neural Stem Cell Transformation to Glioma Stem Cells 
 Shuang Liu, Jianning Zhang, Max S. Wicha, Alfred E. Chang, Wenhong Fan, Ling Chen, Ming Fan, Qiao Li, Feng Yin
  Abstract
To investigate the expressional alternation of microRNAs (miRNA) during the malignant transformation and development of human glioma, we measuredmiRNA expression profile as well as mRNA expression profile in normal human neural stem cells (hNSCs) and human glioma stem cells (hGSCs). We found 116 miRNA up-regulated and 62 miRNA down-regulated in GSCs. On the other hand, we identified 1,372 mRNA down-regulated, and 1,501 mRNA up-regulated in GSCs compared to those in NSCs. We then analyzed the pathways and the predicted target genes of the miRNAs which differ significantly in expression between GSCs and NSCs using the statistical enrichment methods. These target mRNAs are involved in many cancer-related signaling pathways, such as cell cycle, axon guidance, glioma development, adhesion junction, MAPK and Wnt signaling. Furthermore, we obtained the differently expressed miRNA-target relationships according to the £c value which is used to calculate the regulation extent of miRNA-target and using the databases of miRanda, Targetscans and Pictar. Among the top 10 miRNA-target relationships, hsa-miR-198 and its potential targeted gene DCX and NNAT were selected for validation, and NNAT was found to be the direct target of miR-198. Finally, the functional roles of miR-155-5p and miR-124-3p whose expressions altered significantly between GSCs and NSCs were addressed. Our results provide new clues for the potential mechanisms involved in the origin and development of glioma. Clinically, the altered miRNAs may serve as potential targets and diagnostic tools for novel therapeutic strategies of glioblastoma.
   

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  ✔本篇論文使用華聯產品:Human OneArray  
 Scientific Reports. 2015, 5:10106. doi: 10.1038/srep10106.
 Characterization of a Self-renewing and Multi-potent Cell Population Isolated from Human Minor Salivary Glands
 
 
 Lin Lu, Yan Li, Ming-juan Du, Chen Zhang, Xiang-yu Zhang, Hai-zhou Tong, Lei Liu, Ting-lu Han, Wan-di Li, Li Yan, Ning-bei Yin, Hai-dong Li, Zhen-min Zhao
  Abstract
Adult stem cells play an important role in maintaining tissue homeostasis. Although these cells are found in many tissues, the presence of stem cells in the human minor salivary glands is not well explored. Using the explant culture method, we isolated a population of cells with self-renewal and differentiation capacities harboring that reside in the human minor salivary glands, called human minor salivary gland mesenchymal stem cells (hMSGMSCs). These cells show embryonic stem cell and mesenchymal stem cell phenotypes. Our results demonstrate that hMSGMSCs have the potential to undergo mesodermal, ectodermal and endodermal differentiation in conditioned culture systems in vitro. Furthermore, in vivo transplantation of hMSGMSCs into SCID mice after partial hepatectomy shows that hMSGMSCs are able to survive and engraft, characterized by the survival of labeled cells and the expression of the hepatocyte markers AFP and KRT18. These data demonstrate the existence of hMSGMSCs and suggest their potential in cell therapy and regenerative medicine.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 Northeast Bioengineering Conference (nebec). 2014 April 25-27.
 FGF2 and oxygen: Regulators of intergrin alpha-11 and extracellular matrix molecules
 
 
 Alexandra Grella, Denis Kole, Tanja Dominko
  Abstract
Recently, derivation and maintenance of pluripotent stem cells has been focused on environmental cues, with emphasis on the role of extracellular matrix (ECM) and adhesion molecules (AM). We have developed a novel approach that allows for induction of stem cell gene expression in human dermal fibroblasts (hDF) without the use of transgenes. By culturing cells in low oxygen (5% O2) with addition of exogenous FGF2 we have shown that hDF in defined culture conditions express stem cell genes and show translation and nuclear translocation of stem cell transcription factors. We have demonstrated that this shift is coupled with an FGF2-dependent down-regulation of the majority of AM and ECM targets; specifically induction of a significant down-regulation of integrin alpha 11 (Itga11) transcript and results in Itga11 loss from focal adhesions. Investigation of the mechanism by which FGF2 may be involved in regulation of Itga11 is being investigated by studying the molecular pathway downstream of FGF2 ligand that may be involved in the loss of Itga11 and associated collagen I attachment. Dissecting the molecular mechanisms involved in regulation through modulation of extracellular environment and its effect on plasticity may provide insight into the acquisition into the mechanisms involved in reprogramming of differentiated cells.
   

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  ✔本篇論文使用華聯產品:Human miRNA OneArray  
 Plos Genetics. PLOS Genetics doi:10.1371/journal.pgen.1005726.
 fMiRNA-192 and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma
 
 
 
  Abstract
Accumulated evidence demonstrated that long non-coding RNAs (lncRNAs) play a pivotal role in tumorigenesis. However, it is still largely unknown how these lncRNAs were regulated by small ncRNAs, such as microRNAs (miRNAs), at the post-transcriptional level. We here use lncRNA HOTTIP as an example to study how miRNAs impact lncRNAs expression and its biological significance in hepatocellular carcinoma (HCC). LncRNA HOTTIP is a vital oncogene in HCC, one of the deadliest cancers worldwide. In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. Consistent with this notion, a significant negative correlation between these miRNAs and HOTTIP exists in HCC tissue specimens. Interestingly, the dysregulation of the three ncRNAs was associated with overall survival of HCC patients. In addition, the posttranscriptional silencing of HOTTIP by miR-192, miR-204 or HOTTIP siRNAs could significantly suppress viability of HCC cells. On the contrary, antagonizing endogenous miR-192 or miR-204 led to increased HOTTIP expression and stimulated cell proliferation. In vivo mouse xenograft model also support the tumor suppressor role of both miRNAs. Besides the known targets (multiple 5’ end HOX A genes, i.e. HOXA13), glutaminase (GLS1) was identified as a potential downstream target of the miR-192/-204-HOTTIP axis in HCC. Considering glutaminolysis as a crucial hallmark of cancer cells and significantly inhibited cell viability after silencingGLS1, we speculate that the miR-192/-204-HOTTIP axis may interrupt HCC glutaminolysis through GLS1 inhibition. These results elucidate that the miR-192/-204-HOTTIP axis might be an important molecular pathway during hepatic cell tumorigenesis. Our data in clinical HCC samples highlight miR-192, miR-204 and HOTTIP with prognostic and potentially therapeutic
   

  ✔本篇論文使用華聯產品:Human miRNA OneArray  
 Prostate. doi: 10.1002/pros.23068. Epub 2015 Aug 26..
 Hsa-miR-146a-5p modulates androgen-independent prostate cancer cells apoptosis by targeting ROCK1
 
 
 
  Abstract
Background MicroRNAs (miRNAs) have been demonstrated playing important roles in the procession of prostate cancer cells transformation from androgen-dependence to androgen-independence. Methods We conducted the miRNA microarray and realtime PCR analyses in both androgen-dependent (ADPC) and androgen-independent prostate cancer (AIPC) tissues. We also explored the role of hsa-miR-146a-5p (miR-146a) in MSKCC prostate cancer clinical database. Moreover, the impact of miR-146a on prostate cancer cells apoptosis were detected by Hoechst staining and fluorescence-activated cell sorter (FACS). Its target is predicted by DIANA LAB online database and the result was assumed by western blotting and luciferase assay. Results We demonstrated that miR-146a was down-regulated in AIPC tissues and cell lines compared to that in the ADPC tissues. In MSKCC data re-analyses, we found that miR-146a was underexpressed in metastatic prostate cancer tissues and those with Gleason score >8, moreover, low level of miR-146a represented a high biochemical relapse rate after radical prostatectomy. In the functional analyses, we transfected miR-146a mimics into CPRC cell lines and found miR-146a induced cells apoptosis. In mechanic analyses, we found that miR-146a inhibited the basal level of Rho-associated, coiled-coil containing protein kinase 1 (ROCK1) expression by targeting its 3'UTR and an inverse correlation of expression between miR-146a and ROCK1 was observed. Moreover, caspase 3 activity was stimulated by miR-146a overexpression. Conclusion miR-146a has a critical role in the process of AIPC prostate cancer cells apoptosis through regulation of ROCK/Caspase 3 pathway. Targeting this pathway may be a promising therapeutic strategy for future personalized anti-cancer treatment.