Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1384489 (Scratch)
 395 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ginsenoside Rd is a protopanaxadiol-type ginsenoside found in ginseng and is the active ingredient in several Oriental herbal medicines. We investigated the effects of ginsenoside Rd on tumor invasion and metastasis in the human hepatocellular carcinoma HepG2 and its possible mechanism of action. HepG2 cells were treated with ginsenoside Rd at different concentrations. Scratch wound and Boyden chamber assays were used to determine the effects of ginsenoside Rd on the migration and invasiveness of HepG2 cells, respectively. The molecular mechanisms by which ginsenoside Rd inhibited the invasion and migration of HepG2 cells were investigated by RT-PCR, Western blotting, gelatin zymography, promoter assay, and treatment with inhibitors of MAPK signaling. Immunofluorescence analysis was conducted to evaluate the effect of ginsenoside Rd on focal adhesion formation in HepG2 cells. Treatment with ginsenoside Rd dose- and time-dependently inhibited the migration and invasion of HepG2 cells. It achieved this by reducing the expression of MMP-1, MMP-2, and MMP-7, by blocking MAPK signaling by inhibiting the phosphorylation of ERK and p38 MAPK, by inhibition of AP-1 activation, and by inducing focal adhesion formation and modulating vinculin localization and expression. Treatment of HepG2 cells with ginsenoside Rd significantly inhibited metastasis, most likely by blocking MMP activation and MAPK signaling pathways involved in cancer cell migration. These findings may be useful for the development of novel chemotherapeutic agents for the treatment of malignant cancers.
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PMID:Anti-metastatic effects of ginsenoside Rd via inactivation of MAPK signaling and induction of focal adhesion formation. 2198 35

The objective of the present study was to observe the effects of silibinin and the p38 mitogen-activated protein kinase (MAPK) signaling pathway inhibitor SB203580 on the migration and invasion capabilities of SGC7901 cells, and to explore the underlying associated mechanisms. Scratch, Transwell and Matrigel invasion assays were performed to study the effects of silibinin on cell migration and invasion. Western blot analysis was used to determine the expression levels of p38MAPK, phosphorylated (p-)p38MAPK, matrix metalloproteinase (MMP)-2 and MMP-9. At the genomic level, quantitative polymerase chain reaction was performed to evaluate the expression levels of MMP-2 and MMP-9. The results of scratch assay indicated that silibinin inhibited the migration capabilities of human gastric cancer SGC7901 cells in a dose-dependent manner. Additionally, Matrigel invasion and Transwell migration assays revealed that silibinin and SB203580 combined treatment significantly reduced the number of invasive cells. Western blot analysis indicated a reduced phosphorylation of p38MAPK without marked changes in p38MAPK expression. In addition, the expression of MMP-2 and MMP-9 significantly decreased in the presence of silibinin, SB203580, and the combination of silibinin and SB203580. In summary, silibinin decreased the invasion and migration abilities of SGC7901 cells by downregulating the expression of MMP-2 and MMP-9 through inhibiting p38MAPK signaling cascades.
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PMID:Silibinin inhibits the migration and invasion of human gastric cancer SGC7901 cells by downregulating MMP-2 and MMP-9 expression via the p38MAPK signaling pathway. 2934 4