News Column

Report Summarizes Cancer Gene Therapy Study Findings from University of Texas School of Medicine

June 23, 2014



By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- New research on Biotechnology is the subject of a report. According to news reporting out of Houston, Texas, by NewsRx editors, research stated, "Emerging evidence implicates the zinc importer ZIP4 as a critical factor that enhances pancreatic cancer proliferation; however, the role of ZIP4 in promoting pancreatic cancer progression by regulating apoptosis requires elucidation. To determine the effect of ZIP4 on apoptosis, we used cell lines where ZIP4 levels were upregulated or silenced in combination with Chelex 100 treatment to deplete intracellular zinc."

Our news journalists obtained a quote from the research from the University of Texas School of Medicine, "Pancreatic cancer xenografts derived from those cells were also included. TUNEL and flow cytometry analysis were used to measure apoptosis and western blotting was used to analyze protein expression for PARP and multiple caspases. Cell cycle profiles were examined by flow cytometry. Zinc depletion by Chelex induced more apoptosis of pancreatic cancer cells in comparison to normal medium, where almost no apoptosis was observed. ZIP4 stably overexpressed MIA PaCa-2 (MIA-ZIP4) cells were more resistant to zinc depletion-induced apoptosis compared with vector control. Conversely, AsPC-1 (AsPC-shZIP4) cells with stable knockdown of ZIP4 were more sensitive to zinc deficiency than control. Resistance to apoptosis mediated by ZIP4 was accomplished by the caspase pathway. In vivo data also confirmed that ZIP4 overexpressed xenografts showed less apoptosis than controls. Cell cycle profiles indicate that silencing of ZIP4 leads to decreased cell population in S phase and G(0)/G(1) arrest. These results described a previously uncharacterized role of ZIP4 in apoptosis resistance and elucidated a novel pathway through which ZIP4 regulates pancreatic cancer growth."

According to the news editors, the research concluded: "This research provides additional evidence for ZIP4 and related signaling cascade as a molecular target for therapeutic intervention in pancreatic cancer."

For more information on this research see: ZIP4 confers resistance to zinc deficiency-induced apoptosis in pancreatic cancer. Cell Cycle, 2014;13(7):1180-1186. Cell Cycle can be contacted at: Landes Bioscience, 1806 Rio Grande St, Austin, TX 78702, USA (see also Biotechnology).

Our news journalists report that additional information may be obtained by contacting X.B. Cui, Univ Texas Med Sch Houston, Div Gastroenterol Hepatol & Nutr, Houston, TX, United States. Additional authors for this research include Y.Q. Zhang, J.X. Yang, X.T. Sun, J.P. Hagan, S. Guha and M. Li.

Keywords for this news article include: Biotechnology, Texas, Houston, Oncology, Apoptosis, Cytometry, Xenograft, United States, Gastroenterology, Pancreatic Cancer, Xenotransplantion, Cancer Gene Therapy, Pancreatic Neoplasms, 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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