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Content Provider | PubMed Central |
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Author | Wang, Lei Shi, Yu Ju, Peijun Liu, Rui Yeo, Siok Ping Xia, Yinyan Hamed, Owlanj Feng, Zhiwei |
Editor | Tan, Ming |
Copyright Year | 2012 |
Abstract | Melanoma is the most dangerous skin cancer due to its highly metastatic potential and resistance to chemotherapy. Currently, there is no effective treatment for melanoma once it is progressed to metastatic stage. Therefore, further study to elucidate the molecular mechanism underlying the metastasis of melanoma cells is urgently required for the improvement of melanoma treatment. In the present study, we found that diphthamide synthesis 3 (Dph3) is involved in the metastasis of B16F10 murine melanoma cells by insertional mutagenesis. We demonstrated that Dph3 disruption impairs the migration of B16F10 murine melanoma cells. The requirement of Dph3 in the migration of melanoma cells was further confirmed by gene silencing with siRNA in vitro. In corresponding to this result, overexpression of Dph3 significantly promoted the migratory ability of B16F10 and B16F0 melanoma cells. Moreover, down regulation of Dph3 expression in B16F10 melanoma cells strikingly inhibits their cellular invasion and metastasis in vivo. Finally, we found that Dph3 promotes melanoma migration and invasion through the AKT signaling pathway. To conclude, our findings suggest a novel mechanism underlying the metastasis of melanoma cells which might serve as a new intervention target for the treatment of melanoma. |
Related Links | http://dx.doi.org/10.1371/journal.pone.0049988 |
Starting Page | 49988 |
File Format | |
ISSN | 19326203 |
e-ISSN | 19326203 |
Journal | PLoS ONE |
Issue Number | 11 |
Volume Number | 7 |
Language | English |
Publisher | Public Library of Science |
Publisher Date | 2012-11-01 |
Access Restriction | Open |
Rights Holder | Public Library of Science |
Subject Keyword | Biochemistry, Genetics and Molecular Biology(all) Agricultural and Biological Sciences(all) Medicine(all) Research in Higher Education |
Content Type | Text |
Resource Type | Article |
Subject | Multidisciplinary |
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