Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: DrugBank:EXPT01586 (G418)
 2,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, it has been suggested that chemokine/receptor interactions determine the destination of the invasive tumor cells in several types of cancer. It has also been proposed that the stromal cell-derived factor-1 (SDF-1; CXCL12)/CXCR4 system might be involved lymph node metastasis in oral squamous cell carcinoma (SCC). In order to further clarify the role of the SDF-1/CXCR4 system in oral SCC, we generated CXCR4 stable transfectants (IH-CXCR4) using oral SCC cells, and compared them to IH, which did not express CXCR4 and which did not have lymph node metastatic potentials in vivo. We introduced enhanced green fluorescent protein (GFP) fused-CXCR4 into IH cells, and detected the GFP fluorescence in the cytoplasm and cell membrane in approximately 60% of the G418-resistant cells. This bulk-transfectant expressed a high level of CXCR4 mRNA and protein, and exhibited the characteristic calcium fluxes and chemotactic activity observed in treatment with SDF-1. SDF-1 biphasically activated extracellular signal-regulated kinase (ERK)1/2, but continuously activated Akt/protein kinase B (PKB) in IH-CXCR4 cells. Most importantly, IH-CXCR4 cells frequently metastasized to the cervical lymph node, but not to the distant organs in the orthotopic inoculation of nude mice. Furthermore, these lymph node metastases were inhibited by the treatment of a mitogen-activated protein kinase/ERK kinase inhibitor, U0126, or a phosphatidylinositol 3 kinase inhibitor, wortmannin. These results indicate that SDF-1/CXCR4 signaling mediates the establishment of lymph node metastasis in oral SCC via ERK1/2 or Akt/PKB pathway.
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PMID:Acquisition of lymph node, but not distant metastatic potentials, by the overexpression of CXCR4 in human oral squamous cell carcinoma. 1549 52

Human phosphatase and tensin homolog (hPTEN) gene was expressed in vascular smooth muscle cells (VSMCs) to study its effect on VSMC proliferation induced in platelet-derived growth factor (PDGF) conditioned medium. After G418 selection, MTT assay was conducted to examine transfected VSMC proliferation induced in human PDGF conditioned medium. We successfully constructed eukaryotic expression vector pcDNA4/myc-His-PTEN and transferred into VSMC cells. We report that in vitro proliferation of VSMC was inhibited in PTEN transfected VSMCs induced in PDGF conditioned medium. RT-PCR and Western blot results indicated significantly high levels of protein kinase B-PKB and nuclear factor kappa B mRNA and protein, respectively, in PDGF group as compared with the control group.
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PMID:Effect of recombinant hPTEN gene expression on PDGF induced VSMC proliferation. 2489 5

Objective To observe the effect of aplysia Ras homolog I (ARHI) gene on human colon cancer cell (SW480) apoptosis. Methods The pcDNA3.1-FLAG-ARHI plasmid was adopted to transfect the SW480 cell line, and G418 screening to obtain stably ARHI-transfected SW480 cells. Reverse transcription PCR and Western blotting were used to detect mRNA and protein expression of ARHI, respectively. The flow cytometry was applied to detect the effect of ARHI overexpression on colon cancer cell apoptosis. The levels of protein kinase B (Akt), phosphorylated Akt (p-Akt), p53 and Bcl-2 were determined by Western blotting. Results SW480 cells stably overexpressing ARHI were successfully established. Cell apoptosis rate in the cells significantly increased. The protein levels of Bcl-2 and p-Akt substantially decreased, whereas the protein expression level of P53 increased; Akt had no obvious changes. Conclusion The overexpression of ARHI promotes colon cancer SW480 cell apoptosis by inhibiting the level of Akt.
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PMID:[Overexpression of aplysia Ras homolog I (ARHI) increases apoptosis in colon cancer SW480 cells]. 2777 44