PubMed:11606073
Annnotations
PubMed_Structured_Abstracts
{"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T1","span":{"begin":134,"end":301},"obj":"OBJECTIVE"},{"id":"T2","span":{"begin":311,"end":1259},"obj":"METHODS"},{"id":"T3","span":{"begin":1269,"end":2428},"obj":"RESULTS"},{"id":"T4","span":{"begin":2442,"end":2636},"obj":"CONCLUSIONS"}],"text":"Hepatocyte growth factor/scatter factor is implicated in the mode of stromal invasion of uterine squamous cervical cancer.\nOBJECTIVE: The purpose of this study was to examine the relationship of hepatocyte growth factor/scatter factor (HGF/SF) to cell motility and invasion in uterine cervical cancer.\nMETHODS: We examined the expression of HGF/SF and its receptor, c-met, in cervical cancer cell lines SKG-IIIa (squamous cell carcinoma) and Hela-S3 (adenocarcinoma) and in stromal cells of the cervical cancer tissue by reverse transcription-polymerase chain reaction. We studied the effect of HGF/SF on invasiveness of SKG-IIIa and Hela-S3 in an invasion model of the modified Boyden chamber method and by electron microscopy. SKG-IIIa cells were also seeded on the thick Matrigel-coated layer to evaluate the invasion patterns in three-dimensional directions. To investigate the mechanism of an inductive effect of HGF/SF on the invasiveness of SKG-IIIa, we examined the effect of HGF/SF on the expression of intercellular adhesion molecule E-cadherin, cell-substrate adhesion molecules CD44, alpha2beta1, and alpha6beta1, and intracellular skeleton fiber actin in SKG-IIIa in cell enzyme-linked immunosorbent assay (ELISA) and immunofluorescence staining.\nRESULTS: HGF/SF messenger RNA (mRNA) was detected in stromal cells, and c-met mRNA was detected in SKG-IIIa and Hela-S3. Hela-S3 that initially showed weak intercellular contact freely invaded the Matrigel-coated multiporous membrane without the addition of HGF/SF. In contrast, SKG-IIIa that initially showed strong intercellular adhesion could invade the membrane after the addition of HGF/SF. The same results were represented by an addition of HECD-1, an anti-human E-cadherin antibody. In an experiment with cell culture in a thick Matrigel layer, control SKG-IIIa showed a mirror-ball-like invasion pattern, whereas HGF/SF-stimulated SKG-IIIa spread horizontally over the membrane and migrated through the membrane holes, presenting a tentacular invasion pattern. Migration of SKG-IIIa under the membrane was confirmed by scanning and transmission electron microscopy. The addition of HGF/SF in cell ELISA assay decreased the expression of E-cadherin and actin in SKG-IIIa, but it did not change the expression of CD44, alpha2beta1, and alpha6beta1. Immunofluorescence staining revealed that the expression of E-cadherin in cell membrane was disturbed by HGF/SF.\nCONCLUSIONS: Our data indicate that HGF/SF produced by stromal cells influences the mode of stromal invasion of squamous cervical cancer by selectively decreasing the expression of both E-cadherin and actin."}
DisGeNET5_gene_disease
{"project":"DisGeNET5_gene_disease","denotations":[{"id":"11606073-0#25#39#gene3082","span":{"begin":1278,"end":1481},"obj":"gene3082"},{"id":"11606073-0#97#121#diseaseC0279671","span":{"begin":2521,"end":2565},"obj":"diseaseC0279671"},{"id":"11606073-2#30#33#gene3082","span":{"begin":341,"end":344},"obj":"gene3082"},{"id":"11606073-2#30#33#gene3082","span":{"begin":341,"end":344},"obj":"gene3082"},{"id":"11606073-2#65#80#diseaseC0007847","span":{"begin":376,"end":391},"obj":"diseaseC0007847"},{"id":"11606073-2#65#80#diseaseC0302592","span":{"begin":376,"end":391},"obj":"diseaseC0302592"},{"id":"11606073-2#65#80#diseaseC4048328","span":{"begin":376,"end":391},"obj":"diseaseC4048328"},{"id":"11606073-2#184#199#diseaseC0007847","span":{"begin":495,"end":510},"obj":"diseaseC0007847"},{"id":"11606073-2#184#199#diseaseC0302592","span":{"begin":495,"end":510},"obj":"diseaseC0302592"},{"id":"11606073-2#184#199#diseaseC4048328","span":{"begin":495,"end":510},"obj":"diseaseC4048328"},{"id":"11606073-2#140#154#diseaseC0001418","span":{"begin":451,"end":465},"obj":"diseaseC0001418"}],"relations":[{"id":"25#39#gene308297#121#diseaseC0279671","pred":"associated_with","subj":"11606073-0#25#39#gene3082","obj":"11606073-0#97#121#diseaseC0279671"},{"id":"30#33#gene308265#80#diseaseC0007847","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#65#80#diseaseC0007847"},{"id":"30#33#gene308265#80#diseaseC0302592","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#65#80#diseaseC0302592"},{"id":"30#33#gene308265#80#diseaseC4048328","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#65#80#diseaseC4048328"},{"id":"30#33#gene3082184#199#diseaseC0007847","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#184#199#diseaseC0007847"},{"id":"30#33#gene3082184#199#diseaseC0302592","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#184#199#diseaseC0302592"},{"id":"30#33#gene3082184#199#diseaseC4048328","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#184#199#diseaseC4048328"},{"id":"30#33#gene3082140#154#diseaseC0001418","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#140#154#diseaseC0001418"},{"id":"30#33#gene308265#80#diseaseC0007847","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#65#80#diseaseC0007847"},{"id":"30#33#gene308265#80#diseaseC0302592","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#65#80#diseaseC0302592"},{"id":"30#33#gene308265#80#diseaseC4048328","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#65#80#diseaseC4048328"},{"id":"30#33#gene3082184#199#diseaseC0007847","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#184#199#diseaseC0007847"},{"id":"30#33#gene3082184#199#diseaseC0302592","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#184#199#diseaseC0302592"},{"id":"30#33#gene3082184#199#diseaseC4048328","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#184#199#diseaseC4048328"},{"id":"30#33#gene3082140#154#diseaseC0001418","pred":"associated_with","subj":"11606073-2#30#33#gene3082","obj":"11606073-2#140#154#diseaseC0001418"}],"text":"Hepatocyte growth factor/scatter factor is implicated in the mode of stromal invasion of uterine squamous cervical cancer.\nOBJECTIVE: The purpose of this study was to examine the relationship of hepatocyte growth factor/scatter factor (HGF/SF) to cell motility and invasion in uterine cervical cancer.\nMETHODS: We examined the expression of HGF/SF and its receptor, c-met, in cervical cancer cell lines SKG-IIIa (squamous cell carcinoma) and Hela-S3 (adenocarcinoma) and in stromal cells of the cervical cancer tissue by reverse transcription-polymerase chain reaction. We studied the effect of HGF/SF on invasiveness of SKG-IIIa and Hela-S3 in an invasion model of the modified Boyden chamber method and by electron microscopy. SKG-IIIa cells were also seeded on the thick Matrigel-coated layer to evaluate the invasion patterns in three-dimensional directions. To investigate the mechanism of an inductive effect of HGF/SF on the invasiveness of SKG-IIIa, we examined the effect of HGF/SF on the expression of intercellular adhesion molecule E-cadherin, cell-substrate adhesion molecules CD44, alpha2beta1, and alpha6beta1, and intracellular skeleton fiber actin in SKG-IIIa in cell enzyme-linked immunosorbent assay (ELISA) and immunofluorescence staining.\nRESULTS: HGF/SF messenger RNA (mRNA) was detected in stromal cells, and c-met mRNA was detected in SKG-IIIa and Hela-S3. Hela-S3 that initially showed weak intercellular contact freely invaded the Matrigel-coated multiporous membrane without the addition of HGF/SF. In contrast, SKG-IIIa that initially showed strong intercellular adhesion could invade the membrane after the addition of HGF/SF. The same results were represented by an addition of HECD-1, an anti-human E-cadherin antibody. In an experiment with cell culture in a thick Matrigel layer, control SKG-IIIa showed a mirror-ball-like invasion pattern, whereas HGF/SF-stimulated SKG-IIIa spread horizontally over the membrane and migrated through the membrane holes, presenting a tentacular invasion pattern. Migration of SKG-IIIa under the membrane was confirmed by scanning and transmission electron microscopy. The addition of HGF/SF in cell ELISA assay decreased the expression of E-cadherin and actin in SKG-IIIa, but it did not change the expression of CD44, alpha2beta1, and alpha6beta1. Immunofluorescence staining revealed that the expression of E-cadherin in cell membrane was disturbed by HGF/SF.\nCONCLUSIONS: Our data indicate that HGF/SF produced by stromal cells influences the mode of stromal invasion of squamous cervical cancer by selectively decreasing the expression of both E-cadherin and actin."}
DisGeNET
{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":0,"end":24},"obj":"gene:3082"},{"id":"T1","span":{"begin":97,"end":121},"obj":"disease:C0279671"},{"id":"T2","span":{"begin":25,"end":39},"obj":"gene:3082"},{"id":"T3","span":{"begin":97,"end":121},"obj":"disease:C0279671"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Hepatocyte growth factor/scatter factor is implicated in the mode of stromal invasion of uterine squamous cervical cancer.\nOBJECTIVE: The purpose of this study was to examine the relationship of hepatocyte growth factor/scatter factor (HGF/SF) to cell motility and invasion in uterine cervical cancer.\nMETHODS: We examined the expression of HGF/SF and its receptor, c-met, in cervical cancer cell lines SKG-IIIa (squamous cell carcinoma) and Hela-S3 (adenocarcinoma) and in stromal cells of the cervical cancer tissue by reverse transcription-polymerase chain reaction. We studied the effect of HGF/SF on invasiveness of SKG-IIIa and Hela-S3 in an invasion model of the modified Boyden chamber method and by electron microscopy. SKG-IIIa cells were also seeded on the thick Matrigel-coated layer to evaluate the invasion patterns in three-dimensional directions. To investigate the mechanism of an inductive effect of HGF/SF on the invasiveness of SKG-IIIa, we examined the effect of HGF/SF on the expression of intercellular adhesion molecule E-cadherin, cell-substrate adhesion molecules CD44, alpha2beta1, and alpha6beta1, and intracellular skeleton fiber actin in SKG-IIIa in cell enzyme-linked immunosorbent assay (ELISA) and immunofluorescence staining.\nRESULTS: HGF/SF messenger RNA (mRNA) was detected in stromal cells, and c-met mRNA was detected in SKG-IIIa and Hela-S3. Hela-S3 that initially showed weak intercellular contact freely invaded the Matrigel-coated multiporous membrane without the addition of HGF/SF. In contrast, SKG-IIIa that initially showed strong intercellular adhesion could invade the membrane after the addition of HGF/SF. The same results were represented by an addition of HECD-1, an anti-human E-cadherin antibody. In an experiment with cell culture in a thick Matrigel layer, control SKG-IIIa showed a mirror-ball-like invasion pattern, whereas HGF/SF-stimulated SKG-IIIa spread horizontally over the membrane and migrated through the membrane holes, presenting a tentacular invasion pattern. Migration of SKG-IIIa under the membrane was confirmed by scanning and transmission electron microscopy. The addition of HGF/SF in cell ELISA assay decreased the expression of E-cadherin and actin in SKG-IIIa, but it did not change the expression of CD44, alpha2beta1, and alpha6beta1. Immunofluorescence staining revealed that the expression of E-cadherin in cell membrane was disturbed by HGF/SF.\nCONCLUSIONS: Our data indicate that HGF/SF produced by stromal cells influences the mode of stromal invasion of squamous cervical cancer by selectively decreasing the expression of both E-cadherin and actin."}