PubMed:22543584 JSONTXT

{"project":"PubMed_ArguminSci","denotations":[{"id":"T1","span":{"begin":138,"end":300},"obj":"DRI_Background"},{"id":"T2","span":{"begin":301,"end":413},"obj":"DRI_Challenge"},{"id":"T3","span":{"begin":414,"end":614},"obj":"DRI_Outcome"},{"id":"T4","span":{"begin":615,"end":722},"obj":"DRI_Outcome"},{"id":"T5","span":{"begin":723,"end":798},"obj":"DRI_Approach"},{"id":"T6","span":{"begin":799,"end":1000},"obj":"DRI_Background"},{"id":"T7","span":{"begin":1001,"end":1063},"obj":"DRI_Background"},{"id":"T8","span":{"begin":1081,"end":1262},"obj":"DRI_Background"},{"id":"T9","span":{"begin":1263,"end":1430},"obj":"DRI_Background"},{"id":"T10","span":{"begin":1431,"end":1722},"obj":"DRI_Background"},{"id":"T11","span":{"begin":1723,"end":1864},"obj":"DRI_Challenge"},{"id":"T12","span":{"begin":1865,"end":1979},"obj":"DRI_Background"}],"text":"Endoplasmic reticulum protein 29 regulates epithelial cell integrity during the mesenchymal-epithelial transition in breast cancer cells.\nThe epithelial-mesenchymal transition (EMT) correlates with disruption of cell-cell adhesion, loss of cell polarity and development of epithelial cell malignancy. Identifying novel molecules that inhibit EMT has profound potential for developing mechanism-based therapeutics. We previously demonstrated that the endoplasmic reticulum protein 29 (ERp29) is a novel factor that can drive mesenchymal-epithelial transition (MET) and induce cell growth arrest in MDA-MB-231 cells. Here, we show that ERp29 is an important molecule in establishing epithelial cell integrity during the MET. We demonstrate that ERp29 regulates MET in a cell context-dependent manner. ERp29 overexpression induced a complete MET in mesenchymal MDA-MB-231 cells through downregulating the expression of transcriptional repressors (for example, Slug, Snai1, ZEB2 and Twist) of E-cadherin. In contrast, overexpression of ERp29 induces incomplete MET in basal-like BT549 cells in which the expression of EMT-related markers (for example, vimentin; cytokeratin 19 (CK19) and E-cadherin) and the transcriptional repressors of E-cadherin were not altered. However, ERp29 overexpression in both cell-types resulted in loss of filamentous stress fibers, formation of cortical actin and restoration of an epithelial phenotype. Mechanistic studies revealed that overexpression of ERp29 in both cell-types upregulated the expression of TJ proteins (zonula-occludens-1 (ZO-1) and occludin) and the core apical-basal polarity proteins (Par3 and Scribble) at the membrane to enhance cell-cell contact and cell polarization. Knockdown of ERp29 in the epithelial MCF-7 cells decreased the expression of these proteins, leading to the disruption of cell-cell adhesion. Taken together, ERp29 is a novel molecule that regulates MET and epithelial cell integrity in breast cancer cells."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":0,"end":32},"obj":"gene:10961"},{"id":"T1","span":{"begin":117,"end":130},"obj":"disease:C0006142"},{"id":"T2","span":{"begin":0,"end":32},"obj":"gene:10961"},{"id":"T3","span":{"begin":117,"end":130},"obj":"disease:C0678222"}],"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":"Endoplasmic reticulum protein 29 regulates epithelial cell integrity during the mesenchymal-epithelial transition in breast cancer cells.\nThe epithelial-mesenchymal transition (EMT) correlates with disruption of cell-cell adhesion, loss of cell polarity and development of epithelial cell malignancy. Identifying novel molecules that inhibit EMT has profound potential for developing mechanism-based therapeutics. We previously demonstrated that the endoplasmic reticulum protein 29 (ERp29) is a novel factor that can drive mesenchymal-epithelial transition (MET) and induce cell growth arrest in MDA-MB-231 cells. Here, we show that ERp29 is an important molecule in establishing epithelial cell integrity during the MET. We demonstrate that ERp29 regulates MET in a cell context-dependent manner. ERp29 overexpression induced a complete MET in mesenchymal MDA-MB-231 cells through downregulating the expression of transcriptional repressors (for example, Slug, Snai1, ZEB2 and Twist) of E-cadherin. In contrast, overexpression of ERp29 induces incomplete MET in basal-like BT549 cells in which the expression of EMT-related markers (for example, vimentin; cytokeratin 19 (CK19) and E-cadherin) and the transcriptional repressors of E-cadherin were not altered. However, ERp29 overexpression in both cell-types resulted in loss of filamentous stress fibers, formation of cortical actin and restoration of an epithelial phenotype. Mechanistic studies revealed that overexpression of ERp29 in both cell-types upregulated the expression of TJ proteins (zonula-occludens-1 (ZO-1) and occludin) and the core apical-basal polarity proteins (Par3 and Scribble) at the membrane to enhance cell-cell contact and cell polarization. Knockdown of ERp29 in the epithelial MCF-7 cells decreased the expression of these proteins, leading to the disruption of cell-cell adhesion. Taken together, ERp29 is a novel molecule that regulates MET and epithelial cell integrity in breast cancer cells."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":1959,"end":1972},"obj":"HP_0003002"},{"id":"T2","span":{"begin":1959,"end":1972},"obj":"HP_0100013"},{"id":"T3","span":{"begin":1966,"end":1972},"obj":"HP_0002664"}],"text":"Endoplasmic reticulum protein 29 regulates epithelial cell integrity during the mesenchymal-epithelial transition in breast cancer cells.\nThe epithelial-mesenchymal transition (EMT) correlates with disruption of cell-cell adhesion, loss of cell polarity and development of epithelial cell malignancy. Identifying novel molecules that inhibit EMT has profound potential for developing mechanism-based therapeutics. We previously demonstrated that the endoplasmic reticulum protein 29 (ERp29) is a novel factor that can drive mesenchymal-epithelial transition (MET) and induce cell growth arrest in MDA-MB-231 cells. Here, we show that ERp29 is an important molecule in establishing epithelial cell integrity during the MET. We demonstrate that ERp29 regulates MET in a cell context-dependent manner. ERp29 overexpression induced a complete MET in mesenchymal MDA-MB-231 cells through downregulating the expression of transcriptional repressors (for example, Slug, Snai1, ZEB2 and Twist) of E-cadherin. In contrast, overexpression of ERp29 induces incomplete MET in basal-like BT549 cells in which the expression of EMT-related markers (for example, vimentin; cytokeratin 19 (CK19) and E-cadherin) and the transcriptional repressors of E-cadherin were not altered. However, ERp29 overexpression in both cell-types resulted in loss of filamentous stress fibers, formation of cortical actin and restoration of an epithelial phenotype. Mechanistic studies revealed that overexpression of ERp29 in both cell-types upregulated the expression of TJ proteins (zonula-occludens-1 (ZO-1) and occludin) and the core apical-basal polarity proteins (Par3 and Scribble) at the membrane to enhance cell-cell contact and cell polarization. Knockdown of ERp29 in the epithelial MCF-7 cells decreased the expression of these proteins, leading to the disruption of cell-cell adhesion. Taken together, ERp29 is a novel molecule that regulates MET and epithelial cell integrity in breast cancer cells."}

{"project":"Allie","denotations":[{"id":"SS1_22543584_1_0","span":{"begin":142,"end":175},"obj":"expanded"},{"id":"SS2_22543584_1_0","span":{"begin":177,"end":180},"obj":"abbr"},{"id":"SS1_22543584_3_0","span":{"begin":450,"end":482},"obj":"expanded"},{"id":"SS2_22543584_3_0","span":{"begin":484,"end":489},"obj":"abbr"},{"id":"SS1_22543584_3_1","span":{"begin":524,"end":557},"obj":"expanded"},{"id":"SS2_22543584_3_1","span":{"begin":559,"end":562},"obj":"abbr"},{"id":"SS1_22543584_7_0","span":{"begin":1158,"end":1172},"obj":"expanded"},{"id":"SS2_22543584_7_0","span":{"begin":1174,"end":1178},"obj":"abbr"},{"id":"SS1_22543584_9_0","span":{"begin":1551,"end":1569},"obj":"expanded"},{"id":"SS2_22543584_9_0","span":{"begin":1571,"end":1575},"obj":"abbr"}],"relations":[{"id":"AE1_22543584_1_0","pred":"abbreviatedTo","subj":"SS1_22543584_1_0","obj":"SS2_22543584_1_0"},{"id":"AE1_22543584_3_0","pred":"abbreviatedTo","subj":"SS1_22543584_3_0","obj":"SS2_22543584_3_0"},{"id":"AE1_22543584_3_1","pred":"abbreviatedTo","subj":"SS1_22543584_3_1","obj":"SS2_22543584_3_1"},{"id":"AE1_22543584_7_0","pred":"abbreviatedTo","subj":"SS1_22543584_7_0","obj":"SS2_22543584_7_0"},{"id":"AE1_22543584_9_0","pred":"abbreviatedTo","subj":"SS1_22543584_9_0","obj":"SS2_22543584_9_0"}],"text":"Endoplasmic reticulum protein 29 regulates epithelial cell integrity during the mesenchymal-epithelial transition in breast cancer cells.\nThe epithelial-mesenchymal transition (EMT) correlates with disruption of cell-cell adhesion, loss of cell polarity and development of epithelial cell malignancy. Identifying novel molecules that inhibit EMT has profound potential for developing mechanism-based therapeutics. We previously demonstrated that the endoplasmic reticulum protein 29 (ERp29) is a novel factor that can drive mesenchymal-epithelial transition (MET) and induce cell growth arrest in MDA-MB-231 cells. Here, we show that ERp29 is an important molecule in establishing epithelial cell integrity during the MET. We demonstrate that ERp29 regulates MET in a cell context-dependent manner. ERp29 overexpression induced a complete MET in mesenchymal MDA-MB-231 cells through downregulating the expression of transcriptional repressors (for example, Slug, Snai1, ZEB2 and Twist) of E-cadherin. In contrast, overexpression of ERp29 induces incomplete MET in basal-like BT549 cells in which the expression of EMT-related markers (for example, vimentin; cytokeratin 19 (CK19) and E-cadherin) and the transcriptional repressors of E-cadherin were not altered. However, ERp29 overexpression in both cell-types resulted in loss of filamentous stress fibers, formation of cortical actin and restoration of an epithelial phenotype. Mechanistic studies revealed that overexpression of ERp29 in both cell-types upregulated the expression of TJ proteins (zonula-occludens-1 (ZO-1) and occludin) and the core apical-basal polarity proteins (Par3 and Scribble) at the membrane to enhance cell-cell contact and cell polarization. Knockdown of ERp29 in the epithelial MCF-7 cells decreased the expression of these proteins, leading to the disruption of cell-cell adhesion. Taken together, ERp29 is a novel molecule that regulates MET and epithelial cell integrity in breast cancer cells."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"22543584-0#0#32#gene10961","span":{"begin":0,"end":32},"obj":"gene10961"},{"id":"22543584-0#117#130#diseaseC0006142","span":{"begin":117,"end":130},"obj":"diseaseC0006142"},{"id":"22543584-0#117#130#diseaseC0678222","span":{"begin":117,"end":130},"obj":"diseaseC0678222"}],"relations":[{"id":"0#32#gene10961117#130#diseaseC0006142","pred":"associated_with","subj":"22543584-0#0#32#gene10961","obj":"22543584-0#117#130#diseaseC0006142"},{"id":"0#32#gene10961117#130#diseaseC0678222","pred":"associated_with","subj":"22543584-0#0#32#gene10961","obj":"22543584-0#117#130#diseaseC0678222"}],"text":"Endoplasmic reticulum protein 29 regulates epithelial cell integrity during the mesenchymal-epithelial transition in breast cancer cells.\nThe epithelial-mesenchymal transition (EMT) correlates with disruption of cell-cell adhesion, loss of cell polarity and development of epithelial cell malignancy. Identifying novel molecules that inhibit EMT has profound potential for developing mechanism-based therapeutics. We previously demonstrated that the endoplasmic reticulum protein 29 (ERp29) is a novel factor that can drive mesenchymal-epithelial transition (MET) and induce cell growth arrest in MDA-MB-231 cells. Here, we show that ERp29 is an important molecule in establishing epithelial cell integrity during the MET. We demonstrate that ERp29 regulates MET in a cell context-dependent manner. ERp29 overexpression induced a complete MET in mesenchymal MDA-MB-231 cells through downregulating the expression of transcriptional repressors (for example, Slug, Snai1, ZEB2 and Twist) of E-cadherin. In contrast, overexpression of ERp29 induces incomplete MET in basal-like BT549 cells in which the expression of EMT-related markers (for example, vimentin; cytokeratin 19 (CK19) and E-cadherin) and the transcriptional repressors of E-cadherin were not altered. However, ERp29 overexpression in both cell-types resulted in loss of filamentous stress fibers, formation of cortical actin and restoration of an epithelial phenotype. Mechanistic studies revealed that overexpression of ERp29 in both cell-types upregulated the expression of TJ proteins (zonula-occludens-1 (ZO-1) and occludin) and the core apical-basal polarity proteins (Par3 and Scribble) at the membrane to enhance cell-cell contact and cell polarization. Knockdown of ERp29 in the epithelial MCF-7 cells decreased the expression of these proteins, leading to the disruption of cell-cell adhesion. Taken together, ERp29 is a novel molecule that regulates MET and epithelial cell integrity in breast cancer cells."}