In vitro suppression of programmed cell death of B cells by tissue inhibitor of metalloproteinases-1.

Guédez, Liliana; Stetler‐Stevenson, William G.; Wolff, Linda; Wang, Jiun; Fukushima, Paula; Mansoor, Adnan; Stetler‐Stevenson, Maryalice

doi:10.1172/jci2881

Cited by 362 publications

(303 citation statements)

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“…However, a number of studies have demonstrated that the level of TIMP-1 is increased in several cancer forms, for example, colorectal and breast cancer and this increase has often been associated with a poor clinical outcome of the cancer patients (Ree et al, 1997;Holten-Andersen et al, 1999McCarthy et al, 1999;Schrohl et al, 2004;Yukawa et al, 2004). This paradoxical finding has been suggested to be the consequence of distinct tumour-stimulating functions demonstrated for TIMP-1, for example, stimulation of proliferation (Hayakawa et al, 1992) and inhibition of apoptosis (Guedez et al, 1998;Li et al, 1999;Murphy et al, 2002;Lee et al, 2003;Liu et al, 2003Liu et al, , 2005Boulday et al, 2004;Murphy et al, 2004).…”

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confidence: 99%

“…The antiapoptotic effect of TIMP-1 induced by various apoptotic agents has been demonstrated in several different cell types such as human breast epithelial cells (Li et al, 1999;Liu et al, 2003Liu et al, , 2005, human breast carcinoma cells (Lee et al, 2003), human endothelial cells (Boulday et al, 2004), hepatic stellate cells (Murphy et al, 2002(Murphy et al, , 2004) and Burkitt's lymphoma cells (Guedez et al, 1998). Of these studies, only Li et al (1999) investigated the association between TIMP-1 level and cell survival following treatment with chemotherapy (adriamycin).…”

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confidence: 99%

“…Furthermore, this cell system can be used to uncover the mechanisms and signalling pathways involved in the TIMP-1-mediated inhibition of apoptosis. Evidence from a number of recent studies suggests that the focal adhesion kinase (FAK)/ phosphatidylinositol-3 kinase (PI-3 kinase)/Akt/Bad/Bcl-X L /Bcl-2 signalling pathway is involved in the TIMP-1-mediated inhibition of apoptosis (Guedez et al, 1998;Li et al, 1999;Lee et al, 2003;Liu et al, 2003Liu et al, , 2005Boulday et al, 2004); however, further studies are still needed to identify the mechanisms involved.…”

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TIMP-1 gene deficiency increases tumour cell sensitivity to chemotherapy-induced apoptosis

et al. 2006

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Tissue inhibitor of metalloproteinases-1 (TIMP-1) is one of four inhibitors of the matrix metalloproteinases, which are capable of degrading most components of the extracellular matrix. However, in recent years, TIMP-1 has been recognised as a multifunctional protein, playing a complex role in cancer. In this regard, several studies have demonstrated an antiapoptotic effect of TIMP-1 in a number of different cell types. Since chemotherapy works by inducing apoptosis in cancer cells, we raised the hypothesis that TIMP-1 promotes resistance against chemotherapeutic drugs. In order to investigate this hypothesis, we have established TIMP-1 genedeficient and TIMP-1 wild-type fibrosarcoma cells from mouse lung tissue. We have characterised these cells with regard to TIMP-1 genotype, TIMP-1 expression, malignant transformation and sensitivity to chemotherapy-induced apoptosis. We show that TIMP-1 gene deficiency increases the response to chemotherapy considerably, confirming that TIMP-1 protects the cells from apoptosis. This is to our knowledge the first study investigating TIMP-1 and chemotherapy-induced apoptosis employing a powerful model system comprising TIMP-1 gene-deficient cells and their genetically identical wild-type controls. For future studies, this cell system can be used to uncover the mechanisms and signalling pathways involved in the TIMP-1-mediated inhibition of apoptosis as well as to investigate the possibility of using TIMP-1 inhibitors to optimise the effect of conventional chemotherapy.

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TIMP-1 gene deficiency increases tumour cell sensitivity to chemotherapy-induced apoptosis

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“…51 In BL cells, overexpression of TIMP-1 leads to the activation and expression of STAT3, and upregulates the expression of BCL-X L , cyclin D2, and CD44. 3,52 Interestingly, BCL-X L is a target protein of activated STAT3 and plays a major role of antiapoptosis. 53 CD44 is also known to promote cell survival by activating the PI-3 kinase/Akt pathway.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathologic implications of tissue inhibitor of metalloproteinase-1-positive diffuse large B-cell lymphoma

Choi

Lee

et al. 2006

Modern Pathology

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The tissue inhibitor of metalloproteinase-1 (TIMP-1) is a stromal factor that promotes plasmablastic differentiation, and the survival of germinal center B-cells. The expression of TIMP-1 is known to be correlated with a subset of non-Hodgkin lymphoma at the mRNA level, and Epstein-Barr virus infection in vitro. To characterize TIMP-1( þ ) diffuse large B-cell lymphoma, TIMP-1 expression was investigated in tissue microarrays from 182 cases of de novo diffuse large B-cell lymphoma and compared with prognostic factors, immunophenotypes, and Epstein-Barr virus infection status. TIMP-1 was expressed not only in tumor cells themselves, in 14 of 182 cases (8%), designated as TIMP-1( þ ) diffuse large B-cell lymphoma, but also in stromal cells like fibroblasts and endothelial cells. In univariate analysis and hierarchical clustering, our findings suggest that TIMP-1 expression may represent a distinct subgroup. In multivariate analysis, TIMP-1( þ ) diffuse large B-cell lymphoma (n ¼ 14) was associated with unfavorable outcomes compared to TIMP-1(À) diffuse large B-cell lymphoma (n ¼ 168) (odds ratio ¼ 2.5, P ¼ 0.049). Together with TIMP-1 expression, age (greater than 60 years), the presence of B-symptoms, abnormal lactate dehydrogenase level, or more advanced stage (III/IV) was correlated with a poor overall survival. However, TIMP-1 expression in diffuse large B-cell lymphoma was not correlated with other prognostic factors including: clinical stage, international prognostic index score, and nongerminal center B-cell phenotype, as well as Epstein-Barr virus infection. Our results suggest that TIMP-1 expression may be an independent negative prognostic factor in patients with diffuse large B-cell lymphoma.

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“…In addition, TIMP-1 controls apoptosis through a non-MMP inhibitory pathway in some lymphoma cell lines (Guedez et al, 1998), and a procathepsin L-TIMP-1 complex enhances steroidogenesis both in testis and ovary (Boujrad et al, 1995). Nonetheless, it remained that timp-1-deficient mice exhibit no specific phenotypes at the testis level with no compensation by TIMP-2 or TIMP-3 (testatin and protease nexin-1 were not studied).…”

Section: Fig 1 Reverse Transcriptase-polymerase Chain Reaction (Rt-mentioning

confidence: 99%

Differential expression of tissue inhibitor of metalloproteinases type 1 (TIMP‐1) during mouse gonad development

Guyot

Magre

Leduque

et al. 2003

Developmental Dynamics

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In mammals, the gene Sry initiates signaling pathways triggering the differentiation of a testis from a sexually indifferent gonad. Assuming that these morphogenetic events may alter the proteolytic balance, the expression of matrix metalloproteinases (MMPs) and inhibitors (TIMPs) was investigated in gonads from 11.5 days postcoitum (dpc) onward, when testicular organogenesis occurs. Whereas selective MMPs and TIMPs (1-3) were detected in undifferentiated gonads (11.5 dpc) and in neonatal testes, a single TIMP (TIMP-1) was expressed in a sexually dimorphic manner from 12.5 dpc onward (i.e., after overt male gonad differentiation), demonstrated by using a semiquantitative reverse transcriptase-polymerase chain reaction and a Western blot analysis. To gain insight into the role of TIMP-1, the expression of gelatinases (mRNA levels and enzyme activity) was monitored. However, no sex differences could be evidenced, indicating that TIMP-1 was not inhibiting this class of MMPs during testis organogenesis. Apart from being an inhibitor of MMPs, TIMP-1 is known to display growth promoting activities. Of interest, testicular TIMP-1 (but not TIMP-2) levels were further enhanced up to 2 weeks of age, consistent with a role in the early postnatal testicular growth. We, therefore, established an organotypic culture system in which seminiferous cords may differentiate de novo and grow, depending on culture conditions. In that system and mimicking the in vivo situation, TIMP-1 immunolocalized strongly within the male gonadal territory and weakly in female gonads, in which no organization was evident. Experiments are now under way to determine to what extent timp-1 is a morphogenic gene involved in seminiferous cord formation and development. Developmental Dynamics 227:357-366, 2003.

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In vitro suppression of programmed cell death of B cells by tissue inhibitor of metalloproteinases-1.

Cited by 362 publications

References 38 publications

TIMP-1 gene deficiency increases tumour cell sensitivity to chemotherapy-induced apoptosis

TIMP-1 gene deficiency increases tumour cell sensitivity to chemotherapy-induced apoptosis

Clinicopathologic implications of tissue inhibitor of metalloproteinase-1-positive diffuse large B-cell lymphoma

Differential expression of tissue inhibitor of metalloproteinases type 1 (TIMP‐1) during mouse gonad development

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