The present study was designed to explore the cross talk between fatty acid synthase (FASN) and HER2 (ErbB2) in ovarian cancer. A total of 60 ovarian cancer patients and 15 normal ovarian tissues were enrolled. Tissue array was conducted by using a tissue microarray instrument. Immunohistochemistry was performed to quantify the expressions of HER2 and FASN. The FASN was detected to be distributed in the cell cytoplasm and was significantly correlated with cancer grade (p = 0.000) and FIGO staging (p = 0.000). Patients with FASN overexpression in ovarian cancer tend to have a worse overall survival rate (p = 0.000). HER2 was also stained to be distributed in the cell cytoplasm associated with higher expression in high-grade cancer. It was also disclosed that FASN expression level is not correlated with HER2 status in ovarian cancer. These results for the first time indicated that a cross talk in FASN and HER2 expressions might be associated with prognosis in malignant ovarian cancer.

J. Neurochem. (2010) 114, 1590–1604. Abstract Alzheimer’s disease is characterized by accumulation and deposition of Aβ peptides in the brain. Aβ deposition generates reactive‐oxygen species (ROS), which are involved in Alzheimer’s inflammatory and neurodegenerative pathology. We have previously observed that, in Alzheimer’s disease brain, ABCG2 is up‐regulated and AP‐1 is activated, but NF‐κB is not activated. In the present study, we examine the roles and mechanism of ABCG2 on ROS generation, inflammatory gene expression and signaling, heme homeostasis and Aβ production in cell models and on inflammatory signaling and Aβ deposition in Abcg2‐knockout and wild‐type mice. Our results show that ABCG2 plays a protective role against oxidative stress by decreasing ROS generation, enhancing antioxidant capacity, regulating heme level, and inhibiting inflammatory response in cell models. ABCG2 inhibits NF‐κB activation but has less effect on AP‐1 activation induced by ROS. This results in inhibition of interleukin‐8 and growth‐related oncogene (GRO) expression induced by ROS via NF‐κB pathway. Abcg2 deficiency increased Aβ deposition and NF‐κB activation in the brains of Abcg2‐knockout mice compared with controls. These findings suggest that ABCG2 may relieve oxidative stress and inflammatory response via inhibiting NF‐κB signaling pathway in cell models and brain tissues and thus may play a potential protective role in Alzheimer’s neuroinflammatory response.

Alterations in MUC expression occur during colorectal tumorigenesis. The transformation process in MC and SRCC may be different from that in the traditional adenoma-carcinoma sequence.

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Intrauterine growth retardation (IUGR) is thought to program insulin resistance, type 2 diabetes and other metabolic diseases in later life. Skeletal muscle is an important tissue involved in regulating the metabolism. We therefore hypothesized that the regulation of glucose- and lipid-related genes in skeletal muscle may contribute to metabolic changes in rats with IUGR. In this study, IUGR rats were bred from pregnant rats fed a protein-restricted (PR) diet. Insulin resistance (IR)-related metabolic parameters and the expression of key regulatory IR genes such as peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) and glucose transporter 4 (GLUT4) were measured in skeletal muscle from 18-month-old female IUGR rats. The methylation status of promoters of PGC-1α and GLUT4 were assessed in the same tissues. During the aging process, IUGR rats exhibited catch-up growth and obesity. In old age, they showed impaired glucose tolerance demonstrated by high glucose and insulin AUC (area under the curve) values. The expression of glucose transporter 4 (GLUT4) and PGC-1α in skeletal muscle was significantly reduced in IUGR rats. Mean CpG island methylation in the PGC-1α promoter sequence was significantly increased. These results suggest that a PR diet during gestation may induce epigenetic changes, such as DNA methylation, in the promoters of specific genes. The changes may affect gene expression and account for the metabolic alterations in female rats with IUGR.