HpSlyD inducing CDX2 and VIL1 expression mediated through TCTP protein may contribute to intestinal metaplasia in the stomach
Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with H. pylori HpslyD -positive strains associated with IM. To further investigate the signalling pathway involved in HpSlyD-induced IM, CDX2 and VIL...
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Published in | Scientific reports Vol. 7; no. 1; pp. 2278 - 14 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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23.05.2017
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Abstract | Helicobacter pylori
infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with
H. pylori HpslyD
-positive strains associated with IM. To further investigate the signalling pathway involved in HpSlyD-induced IM, CDX2 and VIL1 expressions were determined before and after HpSlyD application. TCTP was knocked down by siRNA or overexpressed by plasmid transfection. An HpSlyD binding protein was used to block HpSlyD’s enzymatic activity. The expression of CDX2 and TCTP in gastric diseases was measured by immunohistochemistry. Our results showed HpSlyD induced CDX2 and VIL1 expressions. TCTP protein expression was markedly increased after application of HpSlyD and in an HpSlyD-expressing stable cell line. Downregulation of TCTP protein led to decreased HpSlyD-induced CDX2 and VIL1. Overexpression of TCTP protein improved the expression of CDX2 and VIL1. Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and TCTP expression. Immunohistochemistry demonstrated that CDX2 and TCTP expression was higher in
HpslyD
-positive specimens compared with
HpslyD
-negative ones. Expression of CDX2 was positively correlated with TCTP in
HpslyD
-positive cells. Our study is the first to show that HpSlyD induction of CDX2 and VIL1 expression mediated through TCTP may contribute to IM in the stomach. |
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AbstractList | Abstract Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with H. pylori HpslyD-positive strains associated with IM. To further investigate the signalling pathway involved in HpSlyD-induced IM, CDX2 and VIL1 expressions were determined before and after HpSlyD application. TCTP was knocked down by siRNA or overexpressed by plasmid transfection. An HpSlyD binding protein was used to block HpSlyD’s enzymatic activity. The expression of CDX2 and TCTP in gastric diseases was measured by immunohistochemistry. Our results showed HpSlyD induced CDX2 and VIL1 expressions. TCTP protein expression was markedly increased after application of HpSlyD and in an HpSlyD-expressing stable cell line. Downregulation of TCTP protein led to decreased HpSlyD-induced CDX2 and VIL1. Overexpression of TCTP protein improved the expression of CDX2 and VIL1. Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and TCTP expression. Immunohistochemistry demonstrated that CDX2 and TCTP expression was higher in HpslyD-positive specimens compared with HpslyD-negative ones. Expression of CDX2 was positively correlated with TCTP in HpslyD-positive cells. Our study is the first to show that HpSlyD induction of CDX2 and VIL1 expression mediated through TCTP may contribute to IM in the stomach. Abstract Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with H. pylori HpslyD -positive strains associated with IM. To further investigate the signalling pathway involved in HpSlyD-induced IM, CDX2 and VIL1 expressions were determined before and after HpSlyD application. TCTP was knocked down by siRNA or overexpressed by plasmid transfection. An HpSlyD binding protein was used to block HpSlyD’s enzymatic activity. The expression of CDX2 and TCTP in gastric diseases was measured by immunohistochemistry. Our results showed HpSlyD induced CDX2 and VIL1 expressions. TCTP protein expression was markedly increased after application of HpSlyD and in an HpSlyD-expressing stable cell line. Downregulation of TCTP protein led to decreased HpSlyD-induced CDX2 and VIL1. Overexpression of TCTP protein improved the expression of CDX2 and VIL1. Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and TCTP expression. Immunohistochemistry demonstrated that CDX2 and TCTP expression was higher in HpslyD -positive specimens compared with HpslyD -negative ones. Expression of CDX2 was positively correlated with TCTP in HpslyD -positive cells. Our study is the first to show that HpSlyD induction of CDX2 and VIL1 expression mediated through TCTP may contribute to IM in the stomach. Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with H. pylori HpslyD -positive strains associated with IM. To further investigate the signalling pathway involved in HpSlyD-induced IM, CDX2 and VIL1 expressions were determined before and after HpSlyD application. TCTP was knocked down by siRNA or overexpressed by plasmid transfection. An HpSlyD binding protein was used to block HpSlyD’s enzymatic activity. The expression of CDX2 and TCTP in gastric diseases was measured by immunohistochemistry. Our results showed HpSlyD induced CDX2 and VIL1 expressions. TCTP protein expression was markedly increased after application of HpSlyD and in an HpSlyD-expressing stable cell line. Downregulation of TCTP protein led to decreased HpSlyD-induced CDX2 and VIL1. Overexpression of TCTP protein improved the expression of CDX2 and VIL1. Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and TCTP expression. Immunohistochemistry demonstrated that CDX2 and TCTP expression was higher in HpslyD -positive specimens compared with HpslyD -negative ones. Expression of CDX2 was positively correlated with TCTP in HpslyD -positive cells. Our study is the first to show that HpSlyD induction of CDX2 and VIL1 expression mediated through TCTP may contribute to IM in the stomach. Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with H. pylori HpslyD-positive strains associated with IM. To further investigate the signalling pathway involved in HpSlyD-induced IM, CDX2 and VIL1 expressions were determined before and after HpSlyD application. TCTP was knocked down by siRNA or overexpressed by plasmid transfection. An HpSlyD binding protein was used to block HpSlyD’s enzymatic activity. The expression of CDX2 and TCTP in gastric diseases was measured by immunohistochemistry. Our results showed HpSlyD induced CDX2 and VIL1 expressions. TCTP protein expression was markedly increased after application of HpSlyD and in an HpSlyD-expressing stable cell line. Downregulation of TCTP protein led to decreased HpSlyD-induced CDX2 and VIL1. Overexpression of TCTP protein improved the expression of CDX2 and VIL1. Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and TCTP expression. Immunohistochemistry demonstrated that CDX2 and TCTP expression was higher in HpslyD-positive specimens compared with HpslyD-negative ones. Expression of CDX2 was positively correlated with TCTP in HpslyD-positive cells. Our study is the first to show that HpSlyD induction of CDX2 and VIL1 expression mediated through TCTP may contribute to IM in the stomach. |
ArticleNumber | 2278 |
Author | Gong, Yuehua Chen, Moye Yuan, Yuan Dong, Nannan Li, Qiuping Liu, Jun Zhu, Yanmei Yu, Xiuwen |
Author_xml | – sequence: 1 givenname: Qiuping surname: Li fullname: Li, Qiuping organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department – sequence: 2 givenname: Yanmei surname: Zhu fullname: Zhu, Yanmei organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Department of Pathology, Cancer Hospital of China Medical University; Liaoning Cancer Hospital & Institute – sequence: 3 givenname: Jun surname: Liu fullname: Liu, Jun organization: Mary Babb Randolph Cancer Center, West Virginia University, Department of Physiology and Pharmacology, West Virginia University – sequence: 4 givenname: Xiuwen surname: Yu fullname: Yu, Xiuwen organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Department of Pathology, Qiqihar Medical College – sequence: 5 givenname: Moye surname: Chen fullname: Chen, Moye organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department – sequence: 6 givenname: Nannan surname: Dong fullname: Dong, Nannan organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department – sequence: 7 givenname: Yuehua surname: Gong fullname: Gong, Yuehua email: yhgong@cmu.edu.cn organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department – sequence: 8 givenname: Yuan surname: Yuan fullname: Yuan, Yuan email: yuanyuan@cmu.edu.cn organization: Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department |
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CitedBy_id | crossref_primary_10_1053_j_gastro_2023_08_028 crossref_primary_10_1136_gutjnl_2017_315318 crossref_primary_10_1186_s12866_019_1517_4 crossref_primary_10_1016_j_ejphar_2020_173566 crossref_primary_10_1186_s12876_021_01678_9 crossref_primary_10_1186_s12935_024_03355_9 crossref_primary_10_1016_j_micpath_2020_104428 crossref_primary_10_1016_j_bspc_2021_103476 |
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Snippet | Helicobacter pylori
infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with
H.... Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection with H.... Abstract Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection... Abstract Helicobacter pylori infection is the most important risk factor for gastric intestinal metaplasia (IM). Our previous study demonstrated that infection... |
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SubjectTerms | 13/1 13/51 38/77 38/90 42/89 631/326/107 692/4020/1503/1504/1829 82/29 82/80 Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism CDX2 protein CDX2 Transcription Factor - genetics CDX2 Transcription Factor - metabolism Cell Line, Tumor Enzymatic activity Gastric Mucosa - metabolism Gastric Mucosa - microbiology Gastric Mucosa - pathology Gene Expression Helicobacter Infections - genetics Helicobacter Infections - metabolism Helicobacter Infections - microbiology Helicobacter pylori Helicobacter pylori - metabolism Helicobacter pylori - physiology Humanities and Social Sciences Humans Immunohistochemistry Intestine Metaplasia Microfilament Proteins - genetics Microfilament Proteins - metabolism multidisciplinary Proteins RNA Interference Science Science (multidisciplinary) Signal transduction siRNA Stomach Stomach - microbiology Stomach - pathology Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - microbiology Tacrolimus Transfection |
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Title | HpSlyD inducing CDX2 and VIL1 expression mediated through TCTP protein may contribute to intestinal metaplasia in the stomach |
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