PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27622658-1 2016 TGFBI has been shown to sensitize ovarian cancer cells to the cytotoxic effects of paclitaxel via an integrin receptor-mediated mechanism that modulates microtubule stability. Paclitaxel 83-93 transforming growth factor beta induced Homo sapiens 0-5 18068629-2 2007 Here, we show that loss of the ECM protein TGFBI (transforming growth factor beta induced) is sufficient to induce specific resistance to paclitaxel and mitotic spindle abnormalities in ovarian cancer cells. Paclitaxel 138-148 transforming growth factor beta induced Homo sapiens 43-48 18068629-2 2007 Here, we show that loss of the ECM protein TGFBI (transforming growth factor beta induced) is sufficient to induce specific resistance to paclitaxel and mitotic spindle abnormalities in ovarian cancer cells. Paclitaxel 138-148 transforming growth factor beta induced Homo sapiens 50-89 18068629-3 2007 Paclitaxel-resistant cells treated with recombinant TGFBI protein show integrin-dependent restoration of paclitaxel sensitivity via FAK- and Rho-dependent stabilization of microtubules. Paclitaxel 0-10 transforming growth factor beta induced Homo sapiens 52-57 18068629-3 2007 Paclitaxel-resistant cells treated with recombinant TGFBI protein show integrin-dependent restoration of paclitaxel sensitivity via FAK- and Rho-dependent stabilization of microtubules. Paclitaxel 105-115 transforming growth factor beta induced Homo sapiens 52-57 18068629-4 2007 Immunohistochemical staining for TGFBI in paclitaxel-treated ovarian cancers from a prospective clinical trial showed that morphological changes of paclitaxel-induced cytotoxicity were restricted to areas of strong expression of TGFBI. Paclitaxel 42-52 transforming growth factor beta induced Homo sapiens 33-38 18068629-4 2007 Immunohistochemical staining for TGFBI in paclitaxel-treated ovarian cancers from a prospective clinical trial showed that morphological changes of paclitaxel-induced cytotoxicity were restricted to areas of strong expression of TGFBI. Paclitaxel 148-158 transforming growth factor beta induced Homo sapiens 33-38 18068629-4 2007 Immunohistochemical staining for TGFBI in paclitaxel-treated ovarian cancers from a prospective clinical trial showed that morphological changes of paclitaxel-induced cytotoxicity were restricted to areas of strong expression of TGFBI. Paclitaxel 148-158 transforming growth factor beta induced Homo sapiens 229-234 28952225-0 2017 VHL-TGFBI signaling is involved in the synergy between 5-aza-2"-deoxycytidine and paclitaxel against human renal cell carcinoma. Paclitaxel 82-92 transforming growth factor beta induced Homo sapiens 4-9 28952225-1 2017 PURPOSE: To analyse the role of von Hippel-Lindau (VHL) and transforming growth factor beta-induced (TGFBI) in synergistic mechanisms of 5-aza-2"-deoxycytidine (DAC) and paclitaxel (PTX) against renal cell carcinoma (RCC). Paclitaxel 170-180 transforming growth factor beta induced Homo sapiens 60-99 28952225-2 2017 METHODS: To elucidate the role in the synergy between DAC and PTX against RCC cells, TGFBI expression was regulated using siRNA technology and an expression vector containing the full-length cDNA for TGFBI was also transfected into RCC cells. Paclitaxel 62-65 transforming growth factor beta induced Homo sapiens 85-90 28952225-4 2017 RESULTS: The results indicated that the expression of TGFBI was significantly decreased by DAC or PTX alone in vitro and in vivo. Paclitaxel 98-101 transforming growth factor beta induced Homo sapiens 54-59 28952225-5 2017 Moreover, the combination of DAC and PTX caused a synergistic decrease in the expression of TGFBI in RCC cells. Paclitaxel 37-40 transforming growth factor beta induced Homo sapiens 92-97 28952225-8 2017 CONCLUSION: Our study suggests that VHL-TGFBI signaling is involved in the synergy between DAC and PTX against RCC cells. Paclitaxel 99-102 transforming growth factor beta induced Homo sapiens 40-45 18068629-0 2007 The extracellular matrix protein TGFBI induces microtubule stabilization and sensitizes ovarian cancers to paclitaxel. Paclitaxel 107-117 transforming growth factor beta induced Homo sapiens 33-38 33987391-0 2021 TGFBI is involved in the formation of polyploid cancer cells and the response to paclitaxel. Paclitaxel 81-91 transforming growth factor beta induced Homo sapiens 0-5 33987391-10 2021 Compared with the empty vector, under paclitaxel treatment, the over-expression of TGFBI in MDA-MB-231 and T-MDA-MB-231 both showed a higher growth inhibition rate. Paclitaxel 38-48 transforming growth factor beta induced Homo sapiens 83-88 33987391-13 2021 Conclusions: TGFBI can increase the sensitivity of paclitaxel in polyploid cancer cells and participate in the formation of polyploidy in MDA-MB-231 induced by nocodazole. Paclitaxel 51-61 transforming growth factor beta induced Homo sapiens 13-18 28534376-0 2017 VHL-TGFBI signaling is involved in the synergy between 5-aza-2"-deoxycytidine and paclitaxel against human renal cell carcinoma. Paclitaxel 82-92 transforming growth factor beta induced Homo sapiens 4-9 28534376-1 2017 PURPOSE: To analyse the role of von Hippel-Lindau (VHL) and transforming growth factor beta-induced (TGFBI) in synergistic mechanisms of 5-aza-2"-deoxycytidine (DAC) and paclitaxel (PTX) against renal cell carcinoma (RCC). Paclitaxel 170-180 transforming growth factor beta induced Homo sapiens 60-99 28534376-2 2017 METHODS: To elucidate the role in the synergy between DAC and PTX against RCC cells, TGFBI expression was regulated using siRNA technology and an expression vector containing the full-length cDNA for TGFBI was also transfected into RCC cells. Paclitaxel 62-65 transforming growth factor beta induced Homo sapiens 85-90 28534376-4 2017 RESULTS: The results indicated that the expression of TGFBI was significantly decreased by DAC or PTX alone in vitro and in vivo. Paclitaxel 98-101 transforming growth factor beta induced Homo sapiens 54-59 28534376-5 2017 Moreover, the combination of DAC and PTX caused a synergistic decrease in the expression of TGFBI in RCC cells. Paclitaxel 37-40 transforming growth factor beta induced Homo sapiens 92-97 28534376-8 2017 CONCLUSIONS: Our study suggests that VHL-TGFBI signaling is involved in the synergy between DAC and PTX against RCC cells. Paclitaxel 100-103 transforming growth factor beta induced Homo sapiens 41-46 26900348-8 2016 RESULTS: We identified 22 TSGs involved in PTX resistance, including BRCA1, TP53, PTEN, APC, CDKN1A, CDKN2A, HIN-1, RASSF1, YAP, ING4, PLK2, FBW7, BLU, LZTS1, REST, FADD, PDCD4, TGFBI, ING1, Bax, PinX1 and hEx. Paclitaxel 43-46 transforming growth factor beta induced Homo sapiens 178-183 22248469-0 2012 TGFBI promoter hypermethylation correlating with paclitaxel chemoresistance in ovarian cancer. Paclitaxel 49-59 transforming growth factor beta induced Homo sapiens 0-5 22640878-1 2012 BACKGROUND: The extracellular matrix (ECM) has a key role in facilitating the progression of ovarian cancer and we have shown recently that the secreted ECM protein TGFBI modulates the response of ovarian cancer to paclitaxel-induced cell death. Paclitaxel 215-225 transforming growth factor beta induced Homo sapiens 165-170 22640878-9 2012 CONCLUSIONS: Therefore, different ECM components use distinct signaling mechanisms in ovarian cancer cells and in particular, TGFBI preferentially interacts through a ss3 integrin receptor mediated mechanism to regulate the response of cells to paclitaxel-induced cell death. Paclitaxel 245-255 transforming growth factor beta induced Homo sapiens 126-131 22248469-1 2012 The purpose of this study is to determine the methylation status of Transforming growth factor-beta-inducible gene-h3 (TGFBI) and its correlation with paclitaxel chemoresistance in ovarian cancer. Paclitaxel 151-161 transforming growth factor beta induced Homo sapiens 68-117 22248469-1 2012 The purpose of this study is to determine the methylation status of Transforming growth factor-beta-inducible gene-h3 (TGFBI) and its correlation with paclitaxel chemoresistance in ovarian cancer. Paclitaxel 151-161 transforming growth factor beta induced Homo sapiens 119-124 22248469-8 2012 The methylation level of TGFBI was significantly higher in paclitaxel resistant cell lines (SKOV3/TR and 2780/TR) than that in the sensitive pairs (P < 0.001). Paclitaxel 59-69 transforming growth factor beta induced Homo sapiens 25-30 22248469-10 2012 However, no statistical differences of relative TGFBI mRNA expression and protein were found in other cells (all P > 0.05), which showed that re-expression of TGFBI could reverse paclitaxel chemoresistance. Paclitaxel 182-192 transforming growth factor beta induced Homo sapiens 162-167 22248469-11 2012 Our results show that TGFBI is frequently methylated and associated with paclitaxel-resistance in ovarian cancer. Paclitaxel 73-83 transforming growth factor beta induced Homo sapiens 22-27 21775522-1 2011 The extracellular matrix protein TGFBI enhances the cytotoxic response of cancer cells to paclitaxel by affecting integrin signals that stabilize microtubules. Paclitaxel 90-100 transforming growth factor beta induced Homo sapiens 33-38 20509890-9 2010 Cells over-expressing TGFBI displayed increased sensitivity to etoposide, paclitaxel, cisplatin and gemcitabine. Paclitaxel 74-84 transforming growth factor beta induced Homo sapiens 22-27