This study was conducted to identify transition characteristics of heavy metal(loid)s and to assess dietary risk in the Angelica gigas and Cnidium officinale grown at the major medicinal plant producing districts in Korea. Average bio-concentration factor (BCF) values and range were 0.056 (0.006-0.511) in arsenic (As), 2.030 (0.021-15.678) in cadmium (Cd), 0.179 (0.052-0.393) in mercury (Hg), and 0.061 (0.013-0.474) in lead (Pb) in Angelica gigas. Average BCF values and range were 0.044 (0.011-0.264) in As, 0.557 (0.052-4.255) in Cd, 0.174 (0.069-0.286) in Hg, and 0.024 (0.012-0.057) in Pb in Cnidium officinale. The BCF values by heavy metal(loid)s in Angelica gigas and Cnidium officinale were high in Cd, copper (Cu) and zinc (Zn), while As and Pb were found to be less transferable. The BCF values calculated in this study will be useful for predicting the uptake of heavy metal(loid)s. Human exposure to As, Cd, Hg, and Pb through dietary intake of Angelica gigas and Cnidium officinale might not cause adverse health effects although some Angelica gigas were higher than the allowable value for Cd. Further study on uptake and accumulation mechanism of Cd by Angelica gigas is required to assess the human health risk associated with soil contamination.
<div>Abstract<p>Lesions of ERBB2, PTEN, and PIK3CA activate the phosphatidylinositol 3-kinase (PI3K) pathway during cancer development by increasing levels of phosphatidylinositol-3,4,5-triphosphate (PIP<sub>3</sub>). 3-Phosphoinositide-dependent kinase 1 (PDK1) is the first node of the PI3K signal output and is required for activation of AKT. PIP<sub>3</sub> recruits PDK1 and AKT to the cell membrane through interactions with their pleckstrin homology domains, allowing PDK1 to activate AKT by phosphorylating it at residue threonine-308. We show that total PDK1 protein and mRNA were overexpressed in a majority of human breast cancers and that 21% of tumors had five or more copies of the gene encoding PDK1, <i>PDPK1</i>. We found that increased <i>PDPK1</i> copy number was associated with upstream pathway lesions (<i>ERBB2</i> amplification, PTEN loss, or <i>PIK3CA</i> mutation), as well as patient survival. Examination of an independent set of breast cancers and tumor cell lines derived from multiple forms of human cancers also found increased PDK1 protein levels associated with such upstream pathway lesions. In human mammary cells, PDK1 enhanced the ability of upstream lesions to signal to AKT, stimulate cell growth and migration, and rendered cells more resistant to PDK1 and PI3K inhibition. After orthotopic transplantation, PDK1 overexpression was not oncogenic but dramatically enhanced the ability of ERBB2 to form tumors. Our studies argue that PDK1 overexpression and increased <i>PDPK1</i> copy number are common occurrences in cancer that potentiate the oncogenic effect of upstream lesions on the PI3K pathway. Therefore, we conclude that alteration of PDK1 is a critical component of oncogenic PI3K signaling in breast cancer. [Cancer Res 2009;69(15):6299–306]</p></div>
Supplementary Information, Methods, Table 1, Figures 1-7 from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma
Supplementary Information, Methods, Table 1, Figures 1-7 from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma
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