Link to PDF download (you have to wait 30 secs and put in a code to download, sorry) http://www.megaupload.com/?d=98L2P6M4
Sciencedaily article on the topic: http://www.sciencedaily.com/releases/2007/11/071112172150.htm
Aberrant expression of zinc transporter ZIP4 (SLC39A4) significantly contributes to human pancreatic cancer pathogenesis and progression
Should be an easy read and it has nice figures
Here is a synopsis, but I’ve left all details of the experiments for the article.
In a variety of tests, Li et al. found zinc transporter ZIP4 to be over-expressed in pancreatic cancer cells (from human pancreatic adenocarcinoma patients, nude mouse model, and pancreatic cancer cell lines). They found 94% of tumors from their patients to have increased ZIP4, suggesting that the presence of ZIP4 might become a source of indicating pancreatic cancer. They also found that cancer proliferation increased when ZIP4 was over expressed compared to the growth of ZIP4(-) controls which suggests that this may provide a target for therapy, as well. Both of these would be of importance as pancreatic cancer currently lacks effective diagnosis and treatment, and, in the words of the authors, pancreatic cancer incidence remains equal to its mortality rate.
Zinc is a critical element for normal cell growth. It is an important enzyme cofactor, hormone regulator (involving GH and IGF-1), and potentially regulates DNA synthesis. Lack of zinc, or problems in zinc uptake, lead to serious health problems due to lack of growth. SLC39A4 (the gene coding for ZIP4) mutations may be the cause for of zinc-deficiency acrodermatitis enteropathica. Too much zinc is toxic, leading to apoptosis, possibly do to zinc influencing endonuclease activity (Sunderman, The influence of zinc on apoptosis).
ZIP4 is the intake transporter of importance just because it happens to be the one of the ZIP family expressed in the pancreas. In another case, low levels of ZnT1 were noticed in mammary gland tumor cells (the ZnT family are involved in zinc efflux and zinc storage).
ZIP4 is from the ZIP family of transporters (Zrt- like, Irt- like proteins… Irt stands for Iron transport, I assume Zrt stands for Zn transport…). They increase zinc uptake and cause release of vesicle-stored intracellular zinc. The increased upregulation of ZIP4 may be necessitated by solid tumors being less able to intake zinc, as well as having a greater than normal requirement of zinc due to their rapid growth rate.
Sciencedaily article on the topic: http://www.sciencedaily.com/releases/2007/11/071112172150.htm
Aberrant expression of zinc transporter ZIP4 (SLC39A4) significantly contributes to human pancreatic cancer pathogenesis and progression
Should be an easy read and it has nice figures
Here is a synopsis, but I’ve left all details of the experiments for the article.
In a variety of tests, Li et al. found zinc transporter ZIP4 to be over-expressed in pancreatic cancer cells (from human pancreatic adenocarcinoma patients, nude mouse model, and pancreatic cancer cell lines). They found 94% of tumors from their patients to have increased ZIP4, suggesting that the presence of ZIP4 might become a source of indicating pancreatic cancer. They also found that cancer proliferation increased when ZIP4 was over expressed compared to the growth of ZIP4(-) controls which suggests that this may provide a target for therapy, as well. Both of these would be of importance as pancreatic cancer currently lacks effective diagnosis and treatment, and, in the words of the authors, pancreatic cancer incidence remains equal to its mortality rate.
Zinc is a critical element for normal cell growth. It is an important enzyme cofactor, hormone regulator (involving GH and IGF-1), and potentially regulates DNA synthesis. Lack of zinc, or problems in zinc uptake, lead to serious health problems due to lack of growth. SLC39A4 (the gene coding for ZIP4) mutations may be the cause for of zinc-deficiency acrodermatitis enteropathica. Too much zinc is toxic, leading to apoptosis, possibly do to zinc influencing endonuclease activity (Sunderman, The influence of zinc on apoptosis).
ZIP4 is the intake transporter of importance just because it happens to be the one of the ZIP family expressed in the pancreas. In another case, low levels of ZnT1 were noticed in mammary gland tumor cells (the ZnT family are involved in zinc efflux and zinc storage).
ZIP4 is from the ZIP family of transporters (Zrt- like, Irt- like proteins… Irt stands for Iron transport, I assume Zrt stands for Zn transport…). They increase zinc uptake and cause release of vesicle-stored intracellular zinc. The increased upregulation of ZIP4 may be necessitated by solid tumors being less able to intake zinc, as well as having a greater than normal requirement of zinc due to their rapid growth rate.
