BIOMAT Database Logo BIOMAT Database Logo

Claudin 1 mediates tumor necrosis factor alpha-induced cell migration in human gastric cancer cells. 2014

Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Atsushi Shiozaki, Hiroki Shimizu, Daisuke Ichikawa, Hirotaka Konishi, Shuhei Komatsu, Takeshi Kubota, Hitoshi Fujiwara, Kazuma Okamoto, Daisuke Iitaka, Shingo Nakashima, Yoshito Nako, Eigo Otsuji, Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

OBJECTIVE To investigate the role of claudin 1 in the regulation of genes involved in cell migration and tumor necrosis factor alpha (TNF-α)-induced gene expression in human gastric adenocarcinoma cells. METHODS Knockdown experiments were conducted with claudin 1 small interfering RNA (siRNA), and the effects on the cell cycle, apoptosis, migration and invasion were analyzed in human gastric adenocarcinoma MKN28 cells. The gene expression profiles of cells were analyzed by microarray and bioinformatics. RESULTS The knockdown of claudin 1 significantly inhibited cell proliferation, migration and invasion, and increased apoptosis. Microarray analysis identified 245 genes whose expression levels were altered by the knockdown of claudin 1. Pathway analysis showed that the top-ranked molecular and cellular function was the cellular movement related pathway, which involved MMP7, TNF-SF10, TGFBR1, and CCL2. Furthermore, TNF- and nuclear frctor-κB were the top-ranked upstream regulators related to claudin 1. TNF-α treatment increased claudin 1 expression and cell migration in MKN28 cells. Microarray analysis indicated that the depletion of claudin 1 inhibited 80% of the TNF-α-induced mRNA expression changes. Further, TNF-α did not enhance cell migration in the claudin 1 siRNA transfected cells. CONCLUSIONS These results suggest that claudin 1 is an important messenger that regulates TNF-α-induced gene expression and migration in gastric cancer cells. A deeper understanding of these cellular processes may be helpful in establishing new therapeutic strategies for gastric cancer.

UI MeSH Term Description Entries
D009361 Neoplasm Invasiveness Ability of neoplasms to infiltrate and actively destroy surrounding tissue. Invasiveness, Neoplasm,Neoplasm Invasion,Invasion, Neoplasm
D002465 Cell Movement The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell. Cell Migration,Locomotion, Cell,Migration, Cell,Motility, Cell,Movement, Cell,Cell Locomotion,Cell Motility,Cell Movements,Movements, Cell
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000230 Adenocarcinoma A malignant epithelial tumor with a glandular organization. Adenocarcinoma, Basal Cell,Adenocarcinoma, Granular Cell,Adenocarcinoma, Oxyphilic,Adenocarcinoma, Tubular,Adenoma, Malignant,Carcinoma, Cribriform,Carcinoma, Granular Cell,Carcinoma, Tubular,Adenocarcinomas,Adenocarcinomas, Basal Cell,Adenocarcinomas, Granular Cell,Adenocarcinomas, Oxyphilic,Adenocarcinomas, Tubular,Adenomas, Malignant,Basal Cell Adenocarcinoma,Basal Cell Adenocarcinomas,Carcinomas, Cribriform,Carcinomas, Granular Cell,Carcinomas, Tubular,Cribriform Carcinoma,Cribriform Carcinomas,Granular Cell Adenocarcinoma,Granular Cell Adenocarcinomas,Granular Cell Carcinoma,Granular Cell Carcinomas,Malignant Adenoma,Malignant Adenomas,Oxyphilic Adenocarcinoma,Oxyphilic Adenocarcinomas,Tubular Adenocarcinoma,Tubular Adenocarcinomas,Tubular Carcinoma,Tubular Carcinomas
D012333 RNA, Messenger RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm. Messenger RNA,Messenger RNA, Polyadenylated,Poly(A) Tail,Poly(A)+ RNA,Poly(A)+ mRNA,RNA, Messenger, Polyadenylated,RNA, Polyadenylated,mRNA,mRNA, Non-Polyadenylated,mRNA, Polyadenylated,Non-Polyadenylated mRNA,Poly(A) RNA,Polyadenylated mRNA,Non Polyadenylated mRNA,Polyadenylated Messenger RNA,Polyadenylated RNA,RNA, Polyadenylated Messenger,mRNA, Non Polyadenylated
D013274 Stomach Neoplasms Tumors or cancer of the STOMACH. Cancer of Stomach,Gastric Cancer,Gastric Neoplasms,Stomach Cancer,Cancer of the Stomach,Gastric Cancer, Familial Diffuse,Neoplasms, Gastric,Neoplasms, Stomach,Cancer, Gastric,Cancer, Stomach,Cancers, Gastric,Cancers, Stomach,Gastric Cancers,Gastric Neoplasm,Neoplasm, Gastric,Neoplasm, Stomach,Stomach Cancers,Stomach Neoplasm
D014162 Transfection The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES. Transfections
D014409 Tumor Necrosis Factor-alpha Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS. Cachectin,TNF-alpha,Tumor Necrosis Factor Ligand Superfamily Member 2,Cachectin-Tumor Necrosis Factor,TNF Superfamily, Member 2,TNFalpha,Tumor Necrosis Factor,Cachectin Tumor Necrosis Factor,Tumor Necrosis Factor alpha
D015398 Signal Transduction The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. Cell Signaling,Receptor-Mediated Signal Transduction,Signal Pathways,Receptor Mediated Signal Transduction,Signal Transduction Pathways,Signal Transduction Systems,Pathway, Signal,Pathway, Signal Transduction,Pathways, Signal,Pathways, Signal Transduction,Receptor-Mediated Signal Transductions,Signal Pathway,Signal Transduction Pathway,Signal Transduction System,Signal Transduction, Receptor-Mediated,Signal Transductions,Signal Transductions, Receptor-Mediated,System, Signal Transduction,Systems, Signal Transduction,Transduction, Signal,Transductions, Signal
D015854 Up-Regulation A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins. Receptor Up-Regulation,Upregulation,Up-Regulation (Physiology),Up Regulation

Related Publications

Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Claudin-1 expression is induced by tumor necrosis factor-alpha in human pancreatic cancer cells.
November 2008, International journal of molecular medicine,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Claudin 1 mediates TNFα-induced gene expression and cell migration in human lung carcinoma cells.
January 2012, PloS one,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Dexamethasone inhibits tumor necrosis factor-alpha-stimulated gastric epithelial cell migration.
October 2009, Journal of the Chinese Medical Association : JCMA,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Hyperthermia enhances tumor necrosis factor alpha-induced apoptosis of a human gastric cancer cell line.
November 2003, Cancer letters,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
cAMP-response element-binding protein mediates tumor necrosis factor-alpha-induced vascular smooth muscle cell migration.
September 2004, Arteriosclerosis, thrombosis, and vascular biology,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
CAMP-response element-binding protein mediates tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 expression in endothelial cells.
January 2006, Hypertension research : official journal of the Japanese Society of Hypertension,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Hypoxia-inducible factor mediates hypoxic and tumor necrosis factor alpha-induced increases in tumor necrosis factor-alpha converting enzyme/ADAM17 expression by synovial cells.
November 2007, The Journal of biological chemistry,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Luteolin sensitizes tumor necrosis factor-alpha-induced apoptosis in human tumor cells.
October 2004, Oncogene,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Claudin-6 enhances cell invasiveness through claudin-1 in AGS human adenocarcinoma gastric cancer cells.
January 2017, Experimental cell research,
Atsushi Shiozaki, and Hiroki Shimizu, and Daisuke Ichikawa, and Hirotaka Konishi, and Shuhei Komatsu, and Takeshi Kubota, and Hitoshi Fujiwara, and Kazuma Okamoto, and Daisuke Iitaka, and Shingo Nakashima, and Yoshito Nako, and Mingyao Liu, and Eigo Otsuji
Tumor necrosis factor alpha induces migration of human eosinophils.
April 1993, Arerugi = [Allergy],
Copied contents to your clipboard!