We are analyzing https://link.springer.com/article/10.1186/1476-4598-4-33.

Title:
Tissue transglutaminase-induced alterations in extracellular matrix inhibit tumor invasion | Molecular Cancer
Description:
Background Alterations in the extracellular matrix (ECM) can affect host-tumor interactions and tumor growth and metastasis. Tissue transglutaminase (TG2, EC 2.3.2.13), a calcium-dependent enzyme that catalyzes covalent cross-linking of proteins, can render the ECM highly stable and resistant to proteolytic degradation. So we determined whether TG2 expression in a tumor or nontumor (stroma) environment could affect the process of metastasis. Two hundred archived samples from patients with breast cancer were studied for the TG2 expression. Also, in an in vitro model the invasive behavior of MDA-MB-231 cells in the presence or absence of exogenous TG2 was determined. Results Tumors associated with negative nodes showed significantly higher expression of TG2 in the stroma (P < 0.001). TG2 in the stroma was catalytically active, as revealed by the presence of isopeptide cross-links. Pretreatment of Matrigel with catalytically active TG2 resulted in strong inhibition of invasion of MDA-MB-231 cells through the Matrigel Transwell filters. Conclusion TG2-induced alterations in the ECM could effectively inhibit the process of metastasis. Therefore, selective induction of catalytically active TG2 at the site of tumor may offer promising approach for limiting the metastasis.
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Keywords {🔍}

tumor, cancer, cells, expression, google, scholar, article, cas, breast, pubmed, stroma, cell, patients, tissue, invasion, ecm, transglutaminase, samples, growth, crosslinking, metastasis, matrigel, mdamb, mehta, extracellular, matrix, proteins, presence, tumors, mmp, active, protein, primary, fig, human, texas, resistant, transwell, metastatic, node, authors, absence, results, figure, incubated, minutes, biol, res, access, affect,

Topics {✒️}

early-stage breast cancer human breast cancer transforming growth factor-beta open access article stetler-stevenson wg drug-resistant breast cancer modulating cell-matrix interactions article download pdf tissue transglutaminase-induced alterations anti-isopeptide monoclonal ab422 breast medical oncology catalyzes covalent cross-linking catalyzes irreversible cross-linking metastatic breast cancer transglutaminase-catalyzed cross-linking multidrug-resistant mcf-7 cells inherently drug-resistant subclones tg2-catalyzed cross-linking tumour-cell invasion human glioma cells paraffin-embedded tumor samples nature rev cancer rabbit anti-tg2 antibody promote wound healing paraffin-embedded tissues breast cancer cells transglutaminase-dependent cross-linking anti-tg2 monoclonal antibodies primary rabbit anti-tg2 mda-mb-231 cultured cells cancer cell growth untreated matrigel-transwell membranes primary breast cancer breast cancer tumors matrigel-coated transwell membrane human subjects methanol/acetic acid solution breast cancer development full size image mol cancer res privacy choices/manage cookies highly invasive adv cancer res tumor cell interactions offer promising approach offer promising approaches promote cell attachment cross-link ecm proteins support cell growth clin cancer res

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Mehta K, Devarajan E, Chen J, Multani A, Pathak S: Multidrug-resistant MCF-7 cells: an identity crisis?

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         headline:Tissue transglutaminase-induced alterations in extracellular matrix inhibit tumor invasion
         description:Alterations in the extracellular matrix (ECM) can affect host-tumor interactions and tumor growth and metastasis. Tissue transglutaminase (TG2, EC 2.3.2.13), a calcium-dependent enzyme that catalyzes covalent cross-linking of proteins, can render the ECM highly stable and resistant to proteolytic degradation. So we determined whether TG2 expression in a tumor or nontumor (stroma) environment could affect the process of metastasis. Two hundred archived samples from patients with breast cancer were studied for the TG2 expression. Also, in an in vitro model the invasive behavior of MDA-MB-231 cells in the presence or absence of exogenous TG2 was determined. Tumors associated with negative nodes showed significantly higher expression of TG2 in the stroma (P < 0.001). TG2 in the stroma was catalytically active, as revealed by the presence of isopeptide cross-links. Pretreatment of Matrigel with catalytically active TG2 resulted in strong inhibition of invasion of MDA-MB-231 cells through the Matrigel Transwell filters. TG2-induced alterations in the ECM could effectively inhibit the process of metastasis. Therefore, selective induction of catalytically active TG2 at the site of tumor may offer promising approach for limiting the metastasis.
         datePublished:2005-09-09T00:00:00Z
         dateModified:2005-09-09T00:00:00Z
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      headline:Tissue transglutaminase-induced alterations in extracellular matrix inhibit tumor invasion
      description:Alterations in the extracellular matrix (ECM) can affect host-tumor interactions and tumor growth and metastasis. Tissue transglutaminase (TG2, EC 2.3.2.13), a calcium-dependent enzyme that catalyzes covalent cross-linking of proteins, can render the ECM highly stable and resistant to proteolytic degradation. So we determined whether TG2 expression in a tumor or nontumor (stroma) environment could affect the process of metastasis. Two hundred archived samples from patients with breast cancer were studied for the TG2 expression. Also, in an in vitro model the invasive behavior of MDA-MB-231 cells in the presence or absence of exogenous TG2 was determined. Tumors associated with negative nodes showed significantly higher expression of TG2 in the stroma (P < 0.001). TG2 in the stroma was catalytically active, as revealed by the presence of isopeptide cross-links. Pretreatment of Matrigel with catalytically active TG2 resulted in strong inhibition of invasion of MDA-MB-231 cells through the Matrigel Transwell filters. TG2-induced alterations in the ECM could effectively inhibit the process of metastasis. Therefore, selective induction of catalytically active TG2 at the site of tumor may offer promising approach for limiting the metastasis.
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         Metastatic Breast Cancer Cell
         Invasive Human Breast Cancer
         Patient Experience Disease Recurrence
         Invasive Human Breast Cancer Cell
         Cancer Research
         Oncology
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