Topic
Cell projection part
About: Cell projection part is a research topic. Over the lifetime, 2 publications have been published within this topic receiving 40 citations.
Papers
TL;DR: The present study showed that leptin and hypoxia altered the profiles of gene expression in L929 cells, which not only extends the cell spectrum of leptin on cell proliferation, but also improves current understanding of hyp oxia in fibroblast cells.
Abstract: Leptin and hypoxia are pro-fibrotic factors involved in fibrogenesis, however, the gene expression profiles remain to be fully elucidated. The aim of the present study was to investigate the regulatory roles of leptin and hypoxia on the L929 mouse fibroblast cell line. The cells were assigned to a normoxia, normoxia with leptin, hypoxia, and hypoxia with leptin group. The cDNA expression was detected using an Agilent mRNA array platform. The differentially expressed genes (DEGs) in response to leptin and hypoxia were identified using reverse transcription‑quantitative polymerase chain reaction analysis, followed by clustering analysis, Gene Ontology analysis and pathway analysis. As a result, 54, 1,507 and 1,502 DEGs were found in response to leptin, hypoxia and the two combined, respectively, among which 52 (96.30%), 467 (30.99%) and 495 (32.96%) of the DEGs were downregulated. The most significant functional terms in response to leptin were meiosis I for biological process (P=0.0041) and synaptonemal complex for cell component (P=0.0013). Only one significant pathway responded to leptin, which was axon guidance (P=0.029). Flow cytometry confirmed that leptin promoted L929 cell proliferation. The most significant functional terms in response to hypoxia were ion binding for molecular function (P=7.8621E‑05), glucose metabolic process for biological process (P=0.0008) and cell projection part for cell component (P=0.003). There were 12 pathways, which significantly responded to hypoxia (P<0.05) and the pathway with the highest significance was the chemokine signaling pathway (P=0.0001), which comprised 28 genes, including C‑C motif ligand (CCL)1, C‑X‑C motif ligand (CXCL)9, CXCL10, son of sevenless homolog 1, AKT serine/threonine kinase 2, Rho‑associated protein kinase 1, vav guanine nucleotide exchange factor 1, CCL17, arrestin β1 and C‑C motif chemokine receptor 2. In conclusion, the present study showed that leptin and hypoxia altered the profiles of gene expression in L929 cells. These findings not only extend the cell spectrum of leptin on cell proliferation, but also improve current understanding of hypoxia in fibroblast cells.
6 citations
TL;DR: This work identified and constructed significant molecule RRM2 phosphoprotein network from 25 no-tumor hepatitis/cirrhotic liver tissues and 25 HCC patients in the same GEO Dataset GSE10140-10141 and deduced the weaker RRM 2 phosphop protein function in HCC consistent with the above computation.
Abstract: RRM2 computational phosphoprotein network construction and analysis of human hepatocellular carcinoma (HCC) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer (GRNInfer) and the database for annotation, visualization and integrated discovery (DAVID) we identified and constructed significant molecule RRM2 phosphoprotein network from 25 no-tumor hepatitis/cirrhotic liver tissues and 25 HCC patients in the same GEO Dataset GSE10140-10141. We gained the negative result of RRM2 phosphoprotein module through the net numbers of activation minus inhibition compared with no-tumor hepatitis/cirrhotic liver tissues and predicted possibly the decrease of RRM2 phosphoprotein module in HCC. Our integrative result showed that RRM2 phosphoprotein cluster of HCC contained both in human no-tumor hepatitis/cirrhotic liver tissues and HCC terms of phosphoprotein (with RRM2) and cell cycle (without RRM2), only in HCC terms of cell-cell signaling, cell projection part, glycoprotein, cell projection, cell adhesion, biological adhesion, integral to plasma membrane, plasma membrane, kinase and phosphorus metabolic process (without RRM2), and none in HCC terms of cell death (without RRM2) and ion binding (with RRM2) compared with human no-tumor hepatitis/cirrhotic liver tissues, all the condition is vital to invasion of HCC. Therefore, we deduced the weaker RRM2 phosphoprotein function in HCC consistent with our above computation. It would be necessary of RRM2 phosphoprotein function decrease to invasion of HCC. RRM2 phosphoprotein interaction module construction in HCC can be a new route for studying the pathogenesis of HCC.
Performance Metrics
| Year | Papers |
|---|---|
| 2017 | 1 |
| 2010 | 1 |