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Studies from Mercer University Yield New Data on Cancer Gene Therapy (Dual modulation of JNK and Akt signaling pathways by chaetoglobosin K in human...

July 14, 2014



Studies from Mercer University Yield New Data on Cancer Gene Therapy (Dual modulation of JNK and Akt signaling pathways by chaetoglobosin K in human lung carcinoma and ras-transformed epithelial cells)

By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- Current study results on Biotechnology have been published. According to news reporting originating from Atlanta, Georgia, by NewsRx correspondents, research stated, "Chaetoglobosin K (ChK) is a natural product that inhibits anchorage-dependent and anchorage-independent growth of ras-transformed cells, prevents tumor-promoter disruption of cell-cell communication, and reduces Akt activation in tumorigenic cells. This study demonstrates how ChK modulates the JNK pathway in ras-transformed and human lung carcinoma cells and investigates regulatory mechanisms controlling ChK's effect on the Akt and JNK signaling pathways."

Our news editors obtained a quote from the research from Mercer University, "Human lung carcinoma and ras-transformed epithelial cell lines treated with ChK or vehicle for varying times were assayed for cell growth or extracted for total proteins for western blot analysis using phosphorylation site-specific antibodies to monitor changes in activation of JNK, Akt, and other signaling enzymes. ChK inhibited both Akt and JNK phosphorylation at key activation sites in ras-transformed cells as well as human lung carcinoma cells. Downstream effectors of both kinases were accordingly affected. Direct upstream kinases of JNK were not affected by ChK. Wortmannin and LY294002, two PI3 kinase inhibitors, inhibited Akt but not JNK phosphorylation in ras-transformed cells. This report establishes the dual inhibitory effect of ChK on both the Akt and JNK signaling pathways in ras-transformed epithelial and human carcinoma cells."

According to the news editors, the research concluded: "The unique effect of ChK on these two key pathways involved in carcinogenesis earmarks ChK for further studies to determine its molecular target(s) and in vivo anti-tumor potential."

For more information on this research see: Dual modulation of JNK and Akt signaling pathways by chaetoglobosin K in human lung carcinoma and ras-transformed epithelial cells. Investigational New Drugs, 2013;31(3):525-34. Investigational New Drugs can be contacted at: Springer, 233 Spring Street, New York, NY 10013, USA. (Springer - www.springer.com; Investigational New Drugs - www.springerlink.com/content/0167-6997/)

The news editors report that additional information may be obtained by contacting A. Ali, Dept. of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, Mercer University, 3001 Mercer University Drive, Atlanta, GA 30341, United States. Additional authors for this research include T.S. Sidorova and D.F Matesic (see also Biotechnology).

Publisher contact information for the journal Investigational New Drugs is: Springer, 233 Spring Street, New York, NY 10013, USA.

Keywords for this news article include: Biotechnology, Atlanta, Georgia, Oncology, Carcinoma, Lung Cancer, United States, Epithelial Cells, Cancer Gene Therapy, North and Central America.

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC


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Source: Cancer Gene Therapy Week


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