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  ✔本篇論文使用華聯產品:Human miRNA OneArray  
 Cellular Physiology And Biochemistry. 2015, 35(6):2169-80. doi: 10.1159/000374022.
 MiR-10b Directly Targets ZEB1 and PIK3CA to Curb Adenomyotic Epithelial Cell Invasiveness via Upregulation of E-Cadherin and Inhibition of Akt Phosphorylation 
 Xiao Lang, Zhen Lu, Jianchao Wang, Ting Li, Ying Loao, Chunyan Jia, Wenxia Zhao, Huiqi Fang, Ying Guo
  Abstract
BACKGROUND/AIMS: Adenomyosis is a disease in which ectopic endometrial glands and stromal cells appear in the uterine myometrium. Despite its prevalence, the molecular mechanisms involved in the development of adenomyosis are largely unknown. The aim of this study was to investigate the role of miR-10b and its target genes ZEB1 and PIK3CA in adenomyosis. METHODS: 1387 miRNAs in human normal endometrium and ectopic endometrial lesions of adenomyosis using a microarray screen assay. The significant differential expression of 10 miRNAs was confirmed by qRT-PCR. The expression of miR-10b in endometrial epithelial cells isolated from normal endometrium and paired eutopic and ectopic endometrium of adenomyosis was measured by qRT-PCR. Subsequently, the targets of miR-10b were predicted by bioinformatics and confirmed using a luciferase assay, and the mRNA and protein expression of ZEB1 and PIK3CA were assessed in the endometrium or endometrial epithelial cells by qRT-PCR and western blotting or immunohistochemical analysis. Cell migration and cell invasion of endometrial epithelial cells with different treatments by Transwell assays. The expression of p-AKT, Akt and E-cadherin proteins was determined by Western blot analysis. RESULTS: MiR-10b expression was significantly downregulated in both adenomyotic lesions and adenomyotic epithelial cells. MiR-10b overexpression in adenomyotic epithelial cells inhibited cell migration and invasion. We then demonstrated that miR-10b directly targets the 3'-UTRs of ZEB1 and PIK3CA, and downregulates ZEB1 and PIK3CA in adenomyotic epithelial cells, leading to increased E-cadherin expression and decreased Akt phosphorylation.
   

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  ✔本篇論文使用華聯產品:Mouse OneArray  
 Molecular And Cellular Endocrinology. 2014, 382(2):804-13. doi: 10.1016/j.mce.2013.10.031.
 Knockdown of TrkA in cumulus oocyte complexes (COCs) inhibits EGF-induced cumulus expansion by down-regulation of IL-6
 
 
 Sun F, Wang Y, Liang N, Yao G, Tian H, Zhai Y, Yin Y
  Abstract
Tyrosine kinase receptor A (TrkA), the high-affinity receptor of nerve growth factor (NGF), is known to play key roles in ovarian follicular development, such as assembly of early follicles and follicular ovulation. However, little is known about the roles of TrkA in cumulus oocyte complex (COC)expansion. In this study, we found that TrkA was abundant in large antral follicles and knockdown of TrkA in COCs attenuated epidermal growth factor (EGF)-induced COC expansion and further decreased the ovulation rate. The effect of TrkA on COC expansion was not mediated through downstream EGF effectors, phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2) or drosophila mothers against decapentaplegic protein (SMAD), or through up-regulation of COC expansion-related transcripts such as prostaglandin-endoperoxide synthase 2 (Ptgs2), hyaluronan synthase 2 (Has2), TNF-induced protein 6 (Tnfaip6) or pentraxin 3 (Ptx3). However, pharmacological blockade of TrkA transducing activity (K252£) in COCsdecreased the mRNA expression and protein secretion of interleukin-6 (IL-6), identified from mRNA microarray of K252£-treated COCs. Meanwhile,knockdown of IL-6 attenuated EGF-induced COC expansion. In addition, IL-6 rescued the inhibitory effect of K252£ on EGF-induced cumulusexpansion. Therefore, IL-6 may act as a new potential cumulus expansion-related transcript, which may be involved in the integration of TrkA and EGF signaling in affecting COC expansion. Here, we provide mechanistic insights into the roles of TrkA in EGF-induced cumulus expansion. Understanding potential cross-points between TrkA and EGF affecting cumulus expansion will help in the discovery of new therapeutic targets in ovulation-related diseases.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 Fertility And Sterility. 2013, 99(7):2000-8.e1. doi: 10.1016/j.fertnstert.2013.01.150.
 Gene expression profiles of cumulus cells obtained from women treated with recombinant human luteinizing hormone + recombinant human follicle-stimulating hormone or highly purified human menopausal gonadotropin versus recombinant human follicle-stimulating hormone alone
 
 
 Tatone C, Ciriminna R, Vento M, Franchi S, D'aurora M, Sperduti S, Cela V, Borzì P, Palermo R, Stuppia L, Artini Pg, Valentina Gatta
  Abstract
OBJECTIVE: To evaluate cumulus cell (CC) expression profile modulation after different stimulation protocols. DESIGN: CCs transcriptome variations were evaluated by microarray in patients undergoing different treatments for ovarian stimulation, namely, r-hLH + r-hFSH and hp-hMG, compared with a control group treated with r-hFSH. SETTING: Healthy patients undergoing assisted reproduction protocols. PATIENT(S): Sixteen healthy women with regular cycles and tubal disease or unexplained infertility. INTERVENTION(S): Four patients received hp-hMG, four received r-hFSH + r-hLH, and eight received r-hFSH daily. Aspiration of the oocytes was performed 36 hours after hCG administration. Only samples derived from cumulus-oocyte complexes containing mature oocytes showing polar body were processed. MAIN OUTCOME MEASURE(S): Comparison of genes differentially expressed in both treatment groups with the use of a hierarchic clustering analysis. RESULT(S): Data clustering analysis allowed detection of four clusters containing genes differentially expressed in both treatment groups compared with control. Functional analysis of the affected transcripts revealed genes involved in oocyte development and maturation. CONCLUSION(S): r-hLH and hCG, though acting on the same receptor, produce a differential activation of intracellular pathways. It can be hypothesized that this effect depends on their different structures and specific binding affinity for the receptor.
   

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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.