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Bioluminescent Orthotopic Model of Pancreatic Cancer Progression
Published on: June 28, 2013
Screening for key lncRNAs in the progression of gallbladder cancer using bioinformatics analyses
Lei Zhang1, Zhimin Geng1, Xiankui Meng1
1Department of Geriatric Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Abstract:
The present study aimed to investigate key long non-coding RNAs (lncRNAs) and genes, and to obtain insights into their roles in the progression of gallbladder cancer (GBC). The gene expression profile and non‑coding RNA profile of GSE62335, which included five separate GBC tissue samples and five matched adjacent gallbladder normal tissue samples, was downloaded from the Gene Expression Omnibus database. The differentially expressed lncRNAs and mRNAs in the GBC tissues were identified, following which RNA binding protein analysis was performed using starBase v2.0 and the co‑expressed lncRNA‑mRNA pairs were predicted. Gene Ontology enrichment analysis for mRNAs was performed using the Database for Annotation Visualization and Integrated Discovery online tool. In addition, upstream microRNAs (miRNAs) were predicted for the co‑expressed lncRNAs and mRNAs. The results revealed that a total of 89 upregulated (13 lncRNAs and 76 mRNAs) and 261 downregulated transcripts (27 lncRNAs and 234 mRNAs) were identified in the GBC tissues. Only 9 lncRNAs had co‑expressed mRNAs, and lncRNA forkhead box P2 (FOXP2) was co‑expressed with the highest number of mRNAs, which were significant associated with the function of cell adhesion. In addition, the analysis of upstream miRNAs showed that FOXF1 adjacent non‑coding developmental regulatory RNA (FENDRR) had common upstream miRNAs, including miR‑18b‑5p, with another 119 differentially expressed genes, and that FENDRR was co‑expressed with adenomatosis polyposis coli downregulated 1 (APCDD1) and v‑kit Hardy‑Zuckerman 4 feline sarcoma viral oncogene homolog (KIT). Taken together, the results suggested that the lncRNAs FOXP2 and FENDRR may be crucial in promoting the progression of GBC via cell adhesion and regulating miR‑18b‑5p, or through interactions with KIT and APCDD1, respectively.
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