Ith TG for 16 or 48 h and total protein per well was measured in cell lysates. N = 3 independent experiments. Bars are SEM. doi:10.1371/journal.pone.0054060.gSupporting InformationFigure S1 Expression of selected ER stress and ECM genes inAcknowledgmentsWe thank Children, comments fellowship Toronto). Dr. James Rutka and Dr. Christian Smith (Hospital for Sick Toronto) for providing the human glioma cell lines and on the manuscript. RNV was funded by a post-doctoral from the Banting and Best Diabetes Centre (University ofhuman glioblastoma multiforme (GBM) tumors (DOCX)Table S1 Expression of selected ER stress and ECM genes inhuman glioblastoma multiforme (GBM) tumors (DOCX)Author ContributionsConceived and designed the experiments: RV AV. Performed the experiments: RV LZ. Analyzed the data: RV LZ AV. Wrote the paper: RV AV.OASIS in Human Glioma Cells
Gastrointestinal tract (GIT) cancer, especially gastric, esophageal and colorectal cancers, are a global epidemiological health concern [1]. There were estimated 1,500,000 new cases of GIT cancer worldwide in 2005 and the number is expected to rise to 2,110,000 in 2025 [2]. Gastric and colon cancers were the second and third most common causes of cancer-related mortality worldwide in 2008, respectively, accounting for over 1 million deaths [3]. Because early-stage esophageal cancer usually does not express symptoms, it has become an aggressive tumor with a dismal 5-year overall survival rate of under 15 [3]. Generally, GIT cancer is known to be a multifactorial disease induced by complex interactions between environmental and genetic factors [4]. Previous studies suggest that lifestyle, dietary and other environmental exposures, and genetic factors might have played a role in causing GIT cancer [5]. However, the majority of genetic variants that influence susceptibility to GIT cancer are still not well-known [6]. Genetic factors may be important contributors to the risk of GIT cancer. Uptill now, a wide range of gastrointestinal cancer susceptibility genes have been identified, including NAT1/ 2, GSTM1, CYP2E1, p53, XRCC1, cyclinD1, IL-1, MMP2,survivin, etc [7?0]. Mutations in these candidate genes have already been linked to elevated risks of developing GIT cancers [11,12]. Survivin, an inhibitor of apoptosis protein (IAP), is involved in the regulation of apoptosis and in cell cycle control [13]. The human survivin gene, located on chromosome 17q25, is approximately 14.7 kbp and consists of 4 exons and 3 introns [14]. Various clinical and experimental studies have shown that increased expression of survivin plays an important role in the development and progression of malignant neoplasms by reducing tumor cell apoptosis [15]. Therefore, survivin can 23977191 be used as a a biomarker and a primary chemotherapeutic target for the detection and treatment of GIT cancer, including esophageal, gastric, and colorectal cancers [16?9]. Different genetic variations located in the regulatory regions of the survivin gene have also been purchase HIF-2��-IN-1 discovered to attribute to the over-expression of survivin. More than 10 common single nucleotide polymorphisms (SNPs) in the promoter region of the survivin gene have been reported, but the 231G.C polymorphism (rs9904341 G.C) is one of the most common variants. The survivin 231G.C polymorphism is a transversion mutation of G to C substitution at position 231 in the promoter region [20]. Recently, many studies have investigatedSurvivin Gene and Gastrointestinal Tract 4EGI-1 Cancerthe.Ith TG for 16 or 48 h and total protein per well was measured in cell lysates. N = 3 independent experiments. Bars are SEM. doi:10.1371/journal.pone.0054060.gSupporting InformationFigure S1 Expression of selected ER stress and ECM genes inAcknowledgmentsWe thank Children, comments fellowship Toronto). Dr. James Rutka and Dr. Christian Smith (Hospital for Sick Toronto) for providing the human glioma cell lines and on the manuscript. RNV was funded by a post-doctoral from the Banting and Best Diabetes Centre (University ofhuman glioblastoma multiforme (GBM) tumors (DOCX)Table S1 Expression of selected ER stress and ECM genes inhuman glioblastoma multiforme (GBM) tumors (DOCX)Author ContributionsConceived and designed the experiments: RV AV. Performed the experiments: RV LZ. Analyzed the data: RV LZ AV. Wrote the paper: RV AV.OASIS in Human Glioma Cells
Gastrointestinal tract (GIT) cancer, especially gastric, esophageal and colorectal cancers, are a global epidemiological health concern [1]. There were estimated 1,500,000 new cases of GIT cancer worldwide in 2005 and the number is expected to rise to 2,110,000 in 2025 [2]. Gastric and colon cancers were the second and third most common causes of cancer-related mortality worldwide in 2008, respectively, accounting for over 1 million deaths [3]. Because early-stage esophageal cancer usually does not express symptoms, it has become an aggressive tumor with a dismal 5-year overall survival rate of under 15 [3]. Generally, GIT cancer is known to be a multifactorial disease induced by complex interactions between environmental and genetic factors [4]. Previous studies suggest that lifestyle, dietary and other environmental exposures, and genetic factors might have played a role in causing GIT cancer [5]. However, the majority of genetic variants that influence susceptibility to GIT cancer are still not well-known [6]. Genetic factors may be important contributors to the risk of GIT cancer. Uptill now, a wide range of gastrointestinal cancer susceptibility genes have been identified, including NAT1/ 2, GSTM1, CYP2E1, p53, XRCC1, cyclinD1, IL-1, MMP2,survivin, etc [7?0]. Mutations in these candidate genes have already been linked to elevated risks of developing GIT cancers [11,12]. Survivin, an inhibitor of apoptosis protein (IAP), is involved in the regulation of apoptosis and in cell cycle control [13]. The human survivin gene, located on chromosome 17q25, is approximately 14.7 kbp and consists of 4 exons and 3 introns [14]. Various clinical and experimental studies have shown that increased expression of survivin plays an important role in the development and progression of malignant neoplasms by reducing tumor cell apoptosis [15]. Therefore, survivin can 23977191 be used as a a biomarker and a primary chemotherapeutic target for the detection and treatment of GIT cancer, including esophageal, gastric, and colorectal cancers [16?9]. Different genetic variations located in the regulatory regions of the survivin gene have also been discovered to attribute to the over-expression of survivin. More than 10 common single nucleotide polymorphisms (SNPs) in the promoter region of the survivin gene have been reported, but the 231G.C polymorphism (rs9904341 G.C) is one of the most common variants. The survivin 231G.C polymorphism is a transversion mutation of G to C substitution at position 231 in the promoter region [20]. Recently, many studies have investigatedSurvivin Gene and Gastrointestinal Tract Cancerthe.