High levels of transglutaminase expression in doxorubicin-resistant human breast carcinoma cells
Tissue type II transglutaminase (TGase) is a member of the TGase family that catalyzes Ca(2+)-dependent covalent cross-linking of several amines to the gamma-carboxamide group of protein-bound glutamine residues. The degree of therapeutic efficacy or toxicity of drugs may be related to their ability to serve as a substrate for TGase and their covalent linkage to glutamine residues of regulatory proteins through the catalytic action of this enzyme. Here, doxorubicin (adriamycin)-resistant human breast carcinoma MCF-7ADR cells exhibited 40- to 6C-fold higher TGase activity than control drug-sensitive MCF-7WT cells. The same was observed in vivo: a small proportion of tumor cells became positive for TGase after administration of adriamycin-based chemotherapy to patients with breast carcinoma. Similarly, continuous culture of MCF-7WT cells in the presence of adriamycin led to the appearance of the drug-resistant phenotype that was in turn associated with increased expression of TGase. This increase in TGase was specific for adriamycin resistance. Like most known TGase, MCF-7ADR TGase was completely dependent on the presence of Ca2+ for its catalytic activity. Based on its immunoreactivity, the TGase in MCF-7ADR cells was identified...Continue Reading
Expression of tissue transglutaminase in Balb-C 3T3 fibroblasts: effects on cellular morphology and adhesion
Re-examination and further development of a precise and rapid dye method for measuring cell growth/cell kill
Similar biochemical changes associated with multidrug resistance in human breast cancer cells and carcinogen-induced resistance to xenobiotics in rats
Formation of a 55 000-weight cross-linked beta crystallin dimer in the Ca2+-treated lens. A model for cataract
Augmentation of adriamycin, melphalan, and cisplatin cytotoxicity in drug-resistant and -sensitive human ovarian carcinoma cell lines by buthionine sulfoximine mediated glutathione depletion
Transglutaminase may mediate certain physiological effects of endogenous amines and of amine-containing therapeutical agents
Removal of the basic center from doxorubicin partially overcomes multidrug resistance and decreases cardiotoxicity
Developmental regulation of tissue transglutaminase during human placentation and expression in neoplastic trophoblast
Transglutaminase 2 cross-linking of matrix proteins: biological significance and medical applications
2-Methoxyestradiol and multidrug resistance: can 2-methoxyestradiol chemosensitize resistant breast cancer cells?
The importance of HER2 signaling in the tumor-initiating cell population in aromatase inhibitor-resistant breast cancer
Ataxia-Telangiectasia, Mutated (ATM)/Nuclear Factor κ light chain enhancer of activated B cells (NFκB) signaling controls basal and DNA damage-induced transglutaminase 2 expression.
Ceramide glycosylation by glucosylceramide synthase selectively maintains the properties of breast cancer stem cells.
Plasma membrane calcium ATPase (PMCA4): a housekeeper for RT-PCR relative quantification of polytopic membrane proteins
Transglutaminase 2 as an independent prognostic marker for survival of patients with non-adenocarcinoma subtype of non-small cell lung cancer
Role of tissue transglutaminase 2 in the acquisition of a mesenchymal-like phenotype in highly invasive A431 tumor cells
Prostate transglutaminase (TGase-4, TGaseP) enhances the adhesion of prostate cancer cells to extracellular matrix, the potential role of TGase-core domain
Down-regulation of extracellular signal-regulated kinase 1/2 activity in P-glycoprotein-mediated multidrug resistant hepatocellular carcinoma cells
Biological functionalities of transglutaminase 2 and the possibility of its compensation by other members of the transglutaminase family
Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway
Eliminating drug resistant breast cancer stem-like cells with combination of simvastatin and gamma-tocotrienol
Depletion of nucleophosmin via transglutaminase 2 cross-linking increases drug resistance in cancer cells
Proteomic analysis of high-molecular-weight protein polymers in a doxorubicin-resistant breast-cancer cell line
Methylglyoxal in cells elicits a negative feedback loop entailing transglutaminase 2 and glyoxalase 1
Lysine residues of IGF-I are substrates for transglutaminases and modulate downstream IGF-I signalling
The opposite effects of doxorubicin on bone marrow stem cells versus breast cancer stem cells depend on glucosylceramide synthase
Calcium blockers decrease the bortezomib resistance in mantle cell lymphoma via manipulation of tissue transglutaminase activities.
The transglutaminase 2 gene (TGM2), a potential molecular marker for chemotherapeutic drug sensitivity, is epigenetically silenced in breast cancer
Implications of increased tissue transglutaminase (TG2) expression in drug-resistant breast cancer (MCF-7) cells
Single-step doxorubicin-selected cancer cells overexpress the ABCG2 drug transporter through epigenetic changes
Cell type-specific activation of intracellular transglutaminase 2 by oxidative stress or ultraviolet irradiation: implications of transglutaminase 2 in age-related cataractogenesis
Transglutaminase 2 inhibitor, KCC009, disrupts fibronectin assembly in the extracellular matrix and sensitizes orthotopic glioblastomas to chemotherapy
Inhibition of Polo-Like Kinase 1 by BI2536 Reverses the Multidrug Resistance of Human Hepatoma Cells In Vitro and In Vivo
Icaritin reverses multidrug resistance of HepG2/ADR human hepatoma cells via downregulation of MDR1 and P‑glycoprotein expression
Trifunctional chemical probes for the consolidated detection and identification of enzyme activities from complex proteomes.
Activation of the Ras-ERK pathway inhibits retinoic acid-induced stimulation of tissue transglutaminase expression in NIH3T3 cells.
Transglutaminase is a mesothelioma cancer stem cell survival protein that is required for tumor formation
PARP3 controls TGFβ and ROS driven epithelial-to-mesenchymal transition and stemness by stimulating a TG2-Snail-E-cadherin axis
Pharmacological separation of the expression of tissue transglutaminase and apoptosis after chemotherapeutic treatment of HepG2 cells
Molecular iodine impairs chemoresistance mechanisms, enhances doxorubicin retention and induces downregulation of the CD44+/CD24+ and E-cadherin+/vimentin+ subpopulations in MCF-7 cells resistant to low doses of doxorubicin
Overexpression of tissue transglutaminase leads to constitutive activation of nuclear factor-kappaB in cancer cells: delineation of a novel pathway
Reversal of drug resistance in breast cancer cells by transglutaminase 2 inhibition and nuclear factor-kappaB inactivation
Augmentation of tissue transglutaminase expression and activation by epidermal growth factor inhibit doxorubicin-induced apoptosis in human breast cancer cells.
Transglutaminase 2 crosslinks the glutathione S-transferase tag, impeding protein-protein interactions of the fused protein.
Breast Cancer: Chemo-Resistance
Some cancers are difficult to treat and aggressive including the "triple-negative" breast cancer. This type of cancer is chemoresistant even before chemotherapy begins. Here are the latest discoveries chemo-resistance in breast cancer.