The Experts below are selected from a list of 846 Experts worldwide ranked by ideXlab platform
Charlotta Enerbäck - One of the best experts on this subject based on the ideXlab platform.
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Loss of ICAM-1 signaling induces psoriasin (S100A7) and MUC1 in mammary epithelial cells
Breast Cancer Research and Treatment, 2011Co-Authors: S. Petersson, Maria Yhr, E. Shubbar, A. Kovacs, Charlotta EnerbäckAbstract:Psoriasin (S100A7), a member of the S100 gene family, is highly expressed in high-grade comedo ductal carcinoma in situ (DCIS), with a higher risk of local recurrence. Psoriasin is, therefore, a potential biomarker for DCIS with a poor prognosis. High-grade DCIS is characterized by a high proliferation rate and crowded cells, consequently, lose contact with the extracellular matrix. The aim of this study was, therefore, to elucidate the involvement of adhesion signals in the regulation of psoriasin. Protein expression was evaluated by Western blotting, flow cytometry, and immunohistochemistry, and using breast carcinoma SAGE databases available from the CGAP website. Intercellular adhesion molecule 1 (ICAM-1) was down-regulated in MCF10A cells using short hairpin RNA. We found a significant negative correlation between the expression of ICAM-1 and psoriasin, and a positive correlation between psoriasin and MUC1 in normal and DCIS SAGE libraries. In a cluster analysis of 34 adhesion molecules and 20 S100 proteins, we showed that SAGE libraries expressing the S100 proteins—psoriasin, Calgranulin-A, and Calgranulin-B—clustered together. Interestingly, the expression of all the three proteins correlated strongly to the oncogenic MUC1. We confirmed the negative correlation between ICAM-1 and psoriasin/MUC1, when normal and breast cancer cells were cultured in suspension and on collagen, respectively. The down-regulation of ICAM-1 by short hairpin RNA in MCF10A cells led to the induction of psoriasin, Calgranulin-A, Calgranulin-B, and MUC1, and we demonstrated that these up-regulations were not ROS dependent. By blocking the phospholipase C (PLC)-IP3 pathway in these cells, we showed that the induction of psoriasin diminished. The results suggest that psoriasin is an intracellular calcium-dependent target of the PLC pathway. Our findings suggest that the down-regulation of ICAM-1 in mammary epithelial cells may contribute both to the high expression of psoriasin seen in some high-grade DCIS tumors and to the induction of MUC1.
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S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells-0
2011Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Copyright information:Taken from "S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells"http://www.biomedcentral.com/1471-2407/7/205BMC Cancer 2007;7():205-205.Published online 6 Nov 2007PMCID:PMC2180183.00 u or 1000 u of IFN-gamma. IFN-gamma treatment had no effect on the protein levels of pro-caspase-3. Calgranulin B and Calgranulin A () are not influenced by the IFN-gamma treatment. Equal amounts of protein lysate were loaded on the gel. , Treatment with 75 μM HOfor one hour followed by culture for 48 h in regular medium induces the expression of Calgranulin A in MCF10A cells. 100 μg of protein lysate were loaded on the gel. , MDA-MB-468 cells with the endogenous expression of psoriasin show the time-dependent repression of psoriasin expression when treated 24, 48 and 72 hours with 1000 u of IFN-gamma. Equal amounts of protein lysate were loaded on the gel. Probing with tubulin/GAPDH assesses the equal loading of the samples. C = cells cultured in monolayer
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S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells-6
2011Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Copyright information:Taken from "S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells"http://www.biomedcentral.com/1471-2407/7/205BMC Cancer 2007;7():205-205.Published online 6 Nov 2007PMCID:PMC2180183.00 u or 1000 u of IFN-gamma. IFN-gamma treatment had no effect on the protein levels of pro-caspase-3. Calgranulin B and Calgranulin A () are not influenced by the IFN-gamma treatment. Equal amounts of protein lysate were loaded on the gel. , Treatment with 75 μM HOfor one hour followed by culture for 48 h in regular medium induces the expression of Calgranulin A in MCF10A cells. 100 μg of protein lysate were loaded on the gel. , MDA-MB-468 cells with the endogenous expression of psoriasin show the time-dependent repression of psoriasin expression when treated 24, 48 and 72 hours with 1000 u of IFN-gamma. Equal amounts of protein lysate were loaded on the gel. Probing with tubulin/GAPDH assesses the equal loading of the samples. C = cells cultured in monolayer
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s100a7 psoriasin highly expressed in ductal carcinoma in situ dcis is regulated by ifn gamma in mammary epithelial cells
BMC Cancer, 2007Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Background The aim of the present work was to explore signal transduction pathways used in the regulation of S100A7 (psoriasin). Members of the S100 gene family participate in many important cellular functions. Psoriasin, S100A8 (Calgranulin A) and S100A9 (Calgranulin B) are expressed in ductal carcinoma in situ (DCIS), as well as in the hyperproliferative skin disease, psoriasis. In the latter condition, a disturbance in the STAT pathway has recently been reported. This pathway is implicated in the regulation of IFN-gamma, widely recognized as a key cytokine in psoriasis. IFN-gamma also exerts anti-tumor action in a number of tumor cell types, including breast cancer. We therefore examined the effect of IFN-gamma and STAT-signaling on the psoriasin expression.
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s100a7 psoriasin highly expressed in ductal carcinoma in situ dcis is regulated by ifn gamma in mammary epithelial cells
BMC Cancer, 2007Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:The aim of the present work was to explore signal transduction pathways used in the regulation of S100A7 (psoriasin). Members of the S100 gene family participate in many important cellular functions. Psoriasin, S100A8 (Calgranulin A) and S100A9 (Calgranulin B) are expressed in ductal carcinoma in situ (DCIS), as well as in the hyperproliferative skin disease, psoriasis. In the latter condition, a disturbance in the STAT pathway has recently been reported. This pathway is implicated in the regulation of IFN-gamma, widely recognized as a key cytokine in psoriasis. IFN-gamma also exerts anti-tumor action in a number of tumor cell types, including breast cancer. We therefore examined the effect of IFN-gamma and STAT-signaling on the psoriasin expression. We established a TAC2 mouse mammary epithelial cell line with tetracycline-inducible psoriasin expression (Tet-Off). Viability in cell culture was estimated using MTS assay. Protein and gene expression were evaluated by Western blotting and quantitative real-time PCR. Statistical analyses were assessed using a one-tailed, paired t-test. We report the downregulation of psoriasin by IFN-gamma in the MDA-MB-468 breast cancer cell line, as well as the downregulation of psoriasin induced by anoikis in cell lines derived from different epithelial tissues. In contrast, IFN-gamma had no suppressive effect on Calgranulin A or Calgranulin B. IFN-gamma is an important activator of the STAT1 pathway and we confirmed an active signaling pathway in the cell lines that responded to IFN-gamma treatment. In contrast, in the SUM190 breast carcinoma cell line, IFN-gamma did not suppress the expression of endogenous psoriasin. Moreover, a reduced phosphorylation of the STAT1 protein was observed. We showed that IFN-gamma treatment and the inhibition of the transcription factor NFkappaB had a synergistic effect on psoriasin levels. Finally, in TAC2 cells with tetracycline-induced psoriasin expression, we observed the increased viability of psoriasin-expressing cells after IFN-gamma treatment. Our data support the possibility that psoriasin expression is transcriptionally suppressed by IFN-gamma and that this effect is likely to be mediated by the activation of the STAT1 signaling pathway. The increased viability of psoriasin-expressing cells after IFN-gamma exposure suggests that psoriasin expression leads to the development of an apoptosis-resistant phenotype.
Maria Yhr - One of the best experts on this subject based on the ideXlab platform.
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Loss of ICAM-1 signaling induces psoriasin (S100A7) and MUC1 in mammary epithelial cells
Breast Cancer Research and Treatment, 2011Co-Authors: S. Petersson, Maria Yhr, E. Shubbar, A. Kovacs, Charlotta EnerbäckAbstract:Psoriasin (S100A7), a member of the S100 gene family, is highly expressed in high-grade comedo ductal carcinoma in situ (DCIS), with a higher risk of local recurrence. Psoriasin is, therefore, a potential biomarker for DCIS with a poor prognosis. High-grade DCIS is characterized by a high proliferation rate and crowded cells, consequently, lose contact with the extracellular matrix. The aim of this study was, therefore, to elucidate the involvement of adhesion signals in the regulation of psoriasin. Protein expression was evaluated by Western blotting, flow cytometry, and immunohistochemistry, and using breast carcinoma SAGE databases available from the CGAP website. Intercellular adhesion molecule 1 (ICAM-1) was down-regulated in MCF10A cells using short hairpin RNA. We found a significant negative correlation between the expression of ICAM-1 and psoriasin, and a positive correlation between psoriasin and MUC1 in normal and DCIS SAGE libraries. In a cluster analysis of 34 adhesion molecules and 20 S100 proteins, we showed that SAGE libraries expressing the S100 proteins—psoriasin, Calgranulin-A, and Calgranulin-B—clustered together. Interestingly, the expression of all the three proteins correlated strongly to the oncogenic MUC1. We confirmed the negative correlation between ICAM-1 and psoriasin/MUC1, when normal and breast cancer cells were cultured in suspension and on collagen, respectively. The down-regulation of ICAM-1 by short hairpin RNA in MCF10A cells led to the induction of psoriasin, Calgranulin-A, Calgranulin-B, and MUC1, and we demonstrated that these up-regulations were not ROS dependent. By blocking the phospholipase C (PLC)-IP3 pathway in these cells, we showed that the induction of psoriasin diminished. The results suggest that psoriasin is an intracellular calcium-dependent target of the PLC pathway. Our findings suggest that the down-regulation of ICAM-1 in mammary epithelial cells may contribute both to the high expression of psoriasin seen in some high-grade DCIS tumors and to the induction of MUC1.
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S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells-0
2011Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Copyright information:Taken from "S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells"http://www.biomedcentral.com/1471-2407/7/205BMC Cancer 2007;7():205-205.Published online 6 Nov 2007PMCID:PMC2180183.00 u or 1000 u of IFN-gamma. IFN-gamma treatment had no effect on the protein levels of pro-caspase-3. Calgranulin B and Calgranulin A () are not influenced by the IFN-gamma treatment. Equal amounts of protein lysate were loaded on the gel. , Treatment with 75 μM HOfor one hour followed by culture for 48 h in regular medium induces the expression of Calgranulin A in MCF10A cells. 100 μg of protein lysate were loaded on the gel. , MDA-MB-468 cells with the endogenous expression of psoriasin show the time-dependent repression of psoriasin expression when treated 24, 48 and 72 hours with 1000 u of IFN-gamma. Equal amounts of protein lysate were loaded on the gel. Probing with tubulin/GAPDH assesses the equal loading of the samples. C = cells cultured in monolayer
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S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells-6
2011Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Copyright information:Taken from "S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells"http://www.biomedcentral.com/1471-2407/7/205BMC Cancer 2007;7():205-205.Published online 6 Nov 2007PMCID:PMC2180183.00 u or 1000 u of IFN-gamma. IFN-gamma treatment had no effect on the protein levels of pro-caspase-3. Calgranulin B and Calgranulin A () are not influenced by the IFN-gamma treatment. Equal amounts of protein lysate were loaded on the gel. , Treatment with 75 μM HOfor one hour followed by culture for 48 h in regular medium induces the expression of Calgranulin A in MCF10A cells. 100 μg of protein lysate were loaded on the gel. , MDA-MB-468 cells with the endogenous expression of psoriasin show the time-dependent repression of psoriasin expression when treated 24, 48 and 72 hours with 1000 u of IFN-gamma. Equal amounts of protein lysate were loaded on the gel. Probing with tubulin/GAPDH assesses the equal loading of the samples. C = cells cultured in monolayer
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s100a7 psoriasin highly expressed in ductal carcinoma in situ dcis is regulated by ifn gamma in mammary epithelial cells
BMC Cancer, 2007Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Background The aim of the present work was to explore signal transduction pathways used in the regulation of S100A7 (psoriasin). Members of the S100 gene family participate in many important cellular functions. Psoriasin, S100A8 (Calgranulin A) and S100A9 (Calgranulin B) are expressed in ductal carcinoma in situ (DCIS), as well as in the hyperproliferative skin disease, psoriasis. In the latter condition, a disturbance in the STAT pathway has recently been reported. This pathway is implicated in the regulation of IFN-gamma, widely recognized as a key cytokine in psoriasis. IFN-gamma also exerts anti-tumor action in a number of tumor cell types, including breast cancer. We therefore examined the effect of IFN-gamma and STAT-signaling on the psoriasin expression.
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s100a7 psoriasin highly expressed in ductal carcinoma in situ dcis is regulated by ifn gamma in mammary epithelial cells
BMC Cancer, 2007Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:The aim of the present work was to explore signal transduction pathways used in the regulation of S100A7 (psoriasin). Members of the S100 gene family participate in many important cellular functions. Psoriasin, S100A8 (Calgranulin A) and S100A9 (Calgranulin B) are expressed in ductal carcinoma in situ (DCIS), as well as in the hyperproliferative skin disease, psoriasis. In the latter condition, a disturbance in the STAT pathway has recently been reported. This pathway is implicated in the regulation of IFN-gamma, widely recognized as a key cytokine in psoriasis. IFN-gamma also exerts anti-tumor action in a number of tumor cell types, including breast cancer. We therefore examined the effect of IFN-gamma and STAT-signaling on the psoriasin expression. We established a TAC2 mouse mammary epithelial cell line with tetracycline-inducible psoriasin expression (Tet-Off). Viability in cell culture was estimated using MTS assay. Protein and gene expression were evaluated by Western blotting and quantitative real-time PCR. Statistical analyses were assessed using a one-tailed, paired t-test. We report the downregulation of psoriasin by IFN-gamma in the MDA-MB-468 breast cancer cell line, as well as the downregulation of psoriasin induced by anoikis in cell lines derived from different epithelial tissues. In contrast, IFN-gamma had no suppressive effect on Calgranulin A or Calgranulin B. IFN-gamma is an important activator of the STAT1 pathway and we confirmed an active signaling pathway in the cell lines that responded to IFN-gamma treatment. In contrast, in the SUM190 breast carcinoma cell line, IFN-gamma did not suppress the expression of endogenous psoriasin. Moreover, a reduced phosphorylation of the STAT1 protein was observed. We showed that IFN-gamma treatment and the inhibition of the transcription factor NFkappaB had a synergistic effect on psoriasin levels. Finally, in TAC2 cells with tetracycline-induced psoriasin expression, we observed the increased viability of psoriasin-expressing cells after IFN-gamma treatment. Our data support the possibility that psoriasin expression is transcriptionally suppressed by IFN-gamma and that this effect is likely to be mediated by the activation of the STAT1 signaling pathway. The increased viability of psoriasin-expressing cells after IFN-gamma exposure suggests that psoriasin expression leads to the development of an apoptosis-resistant phenotype.
Stina Petersson - One of the best experts on this subject based on the ideXlab platform.
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S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells-0
2011Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Copyright information:Taken from "S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells"http://www.biomedcentral.com/1471-2407/7/205BMC Cancer 2007;7():205-205.Published online 6 Nov 2007PMCID:PMC2180183.00 u or 1000 u of IFN-gamma. IFN-gamma treatment had no effect on the protein levels of pro-caspase-3. Calgranulin B and Calgranulin A () are not influenced by the IFN-gamma treatment. Equal amounts of protein lysate were loaded on the gel. , Treatment with 75 μM HOfor one hour followed by culture for 48 h in regular medium induces the expression of Calgranulin A in MCF10A cells. 100 μg of protein lysate were loaded on the gel. , MDA-MB-468 cells with the endogenous expression of psoriasin show the time-dependent repression of psoriasin expression when treated 24, 48 and 72 hours with 1000 u of IFN-gamma. Equal amounts of protein lysate were loaded on the gel. Probing with tubulin/GAPDH assesses the equal loading of the samples. C = cells cultured in monolayer
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S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells-6
2011Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Copyright information:Taken from "S100A7 (Psoriasin), highly expressed in Ductal Carcinoma (DCIS), is regulated by IFN-gamma in mammary epithelial cells"http://www.biomedcentral.com/1471-2407/7/205BMC Cancer 2007;7():205-205.Published online 6 Nov 2007PMCID:PMC2180183.00 u or 1000 u of IFN-gamma. IFN-gamma treatment had no effect on the protein levels of pro-caspase-3. Calgranulin B and Calgranulin A () are not influenced by the IFN-gamma treatment. Equal amounts of protein lysate were loaded on the gel. , Treatment with 75 μM HOfor one hour followed by culture for 48 h in regular medium induces the expression of Calgranulin A in MCF10A cells. 100 μg of protein lysate were loaded on the gel. , MDA-MB-468 cells with the endogenous expression of psoriasin show the time-dependent repression of psoriasin expression when treated 24, 48 and 72 hours with 1000 u of IFN-gamma. Equal amounts of protein lysate were loaded on the gel. Probing with tubulin/GAPDH assesses the equal loading of the samples. C = cells cultured in monolayer
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s100a7 psoriasin highly expressed in ductal carcinoma in situ dcis is regulated by ifn gamma in mammary epithelial cells
BMC Cancer, 2007Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:Background The aim of the present work was to explore signal transduction pathways used in the regulation of S100A7 (psoriasin). Members of the S100 gene family participate in many important cellular functions. Psoriasin, S100A8 (Calgranulin A) and S100A9 (Calgranulin B) are expressed in ductal carcinoma in situ (DCIS), as well as in the hyperproliferative skin disease, psoriasis. In the latter condition, a disturbance in the STAT pathway has recently been reported. This pathway is implicated in the regulation of IFN-gamma, widely recognized as a key cytokine in psoriasis. IFN-gamma also exerts anti-tumor action in a number of tumor cell types, including breast cancer. We therefore examined the effect of IFN-gamma and STAT-signaling on the psoriasin expression.
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s100a7 psoriasin highly expressed in ductal carcinoma in situ dcis is regulated by ifn gamma in mammary epithelial cells
BMC Cancer, 2007Co-Authors: Stina Petersson, Anna Bylander, Maria Yhr, Charlotta EnerbäckAbstract:The aim of the present work was to explore signal transduction pathways used in the regulation of S100A7 (psoriasin). Members of the S100 gene family participate in many important cellular functions. Psoriasin, S100A8 (Calgranulin A) and S100A9 (Calgranulin B) are expressed in ductal carcinoma in situ (DCIS), as well as in the hyperproliferative skin disease, psoriasis. In the latter condition, a disturbance in the STAT pathway has recently been reported. This pathway is implicated in the regulation of IFN-gamma, widely recognized as a key cytokine in psoriasis. IFN-gamma also exerts anti-tumor action in a number of tumor cell types, including breast cancer. We therefore examined the effect of IFN-gamma and STAT-signaling on the psoriasin expression. We established a TAC2 mouse mammary epithelial cell line with tetracycline-inducible psoriasin expression (Tet-Off). Viability in cell culture was estimated using MTS assay. Protein and gene expression were evaluated by Western blotting and quantitative real-time PCR. Statistical analyses were assessed using a one-tailed, paired t-test. We report the downregulation of psoriasin by IFN-gamma in the MDA-MB-468 breast cancer cell line, as well as the downregulation of psoriasin induced by anoikis in cell lines derived from different epithelial tissues. In contrast, IFN-gamma had no suppressive effect on Calgranulin A or Calgranulin B. IFN-gamma is an important activator of the STAT1 pathway and we confirmed an active signaling pathway in the cell lines that responded to IFN-gamma treatment. In contrast, in the SUM190 breast carcinoma cell line, IFN-gamma did not suppress the expression of endogenous psoriasin. Moreover, a reduced phosphorylation of the STAT1 protein was observed. We showed that IFN-gamma treatment and the inhibition of the transcription factor NFkappaB had a synergistic effect on psoriasin levels. Finally, in TAC2 cells with tetracycline-induced psoriasin expression, we observed the increased viability of psoriasin-expressing cells after IFN-gamma treatment. Our data support the possibility that psoriasin expression is transcriptionally suppressed by IFN-gamma and that this effect is likely to be mediated by the activation of the STAT1 signaling pathway. The increased viability of psoriasin-expressing cells after IFN-gamma exposure suggests that psoriasin expression leads to the development of an apoptosis-resistant phenotype.
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psoriasin s100a7 and Calgranulin b s100a9 induction is dependent on reactive oxygen species and is downregulated by bcl 2 and antioxidants
Cancer Biology & Therapy, 2005Co-Authors: Hanna Carlsson, Stina Petersson, Maria Yhr, Nicole Collins, Kornelia Polyak, Charlotta EnerbäckAbstract:S-100 proteins are calcium-binding proteins with important growth regulatory functions. Of these proteins, psoriasin and Calgranulin-B have been shown to be highly upregulated in ductal carcinoma in situ (DCIS) of the breast and in psoriasis. The purpose of this study was to further elucidate the functional relevance of the overexpression of these two S-100 proteins in psoriasis and DCIS. We report the induction of both proteins by reactive oxygen species, phorbol ester TPA, and the induction of psoriasin in response to the PI3K inhibitor wortmannin. We also demonstrate that Bcl-2 overexpression represses the induction of psoriasin and Calgranulin-B under these different conditions. The same effect was obtained with the antioxidant NAC, which indicates that the suppression of psoriasin and Calgranulin-B induction is mediated by the antioxidant function of Bcl-2. Furthermore, we demonstrate that overexpression of a dominant negative IKKβ also inhibits the induction of psoriasin suggesting that the NFκB pathway is involved in the induction of this protein. Also, we found NFκB responsive DNA elements in the upstream promoter region of psoriasin. MCF10A cells with a stable retroviral overexpression of psoriasin were significantly more resistant to H 2 O 2 -induced cell death than control cells further supporting the hypothesis that these S-100 proteins may play a role in oxidative stress response.
Byong Chul Yoo - One of the best experts on this subject based on the ideXlab platform.
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Identification of Calgranulin B interacting proteins and network analysis in gastrointestinal cancer cells.
PloS one, 2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:Calgranulin B is known to be involved in tumor development, but the underlying molecular mechanism is not clear. To gain insight into possible roles of Calgranulin B, we screened for Calgranulin B-interacting molecules in the SNU-484 gastric cancer and the SNU-81 colon cancer cells. Calgranulin B-interacting partners were identified by yeast two-hybrid and functional information was obtained by computational analysis. Most of the Calgranulin B-interacting partners were involved in metabolic and cellular processes, and found to have molecular function of binding and catalytic activities. Interestingly, 46 molecules in the network of the Calgranulin B-interacting proteins are known to be associated with cancer and FKBP2 was found to interact with Calgranulin B in both SNU-484 and SNU-81 cells. Polyubiquitin-C encoded by UBC, which exhibited an interaction with Calgranulin B, has been associated with various molecules of the extracellular space and plasma membrane identified in our screening, including Na-K-Cl cotransporter 1 and dystonin in SNU-484 cells, and ATPase subunit beta-1 in SNU-81 cells. Our data provide novel insight into the roles of Calgranulin B of gastrointestinal cancer cells, and offer new clues suggesting Calgranulin B acts as an effector molecule through which the cell can communicate with the tumor microenvironment via polyubiquitin-C.
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PANTHER analysis of protein classes overrepresented among the Calgranulin B-interacting partners.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:Protein class distributions of the Calgranulin B-interacting molecules identified in SNU-484 (A), SNU-81 (B), and HEK293 (C) cells are shown.
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Communication of Calgranulin B with extracellular environment via polyubiquitin-C(UBC) in SNU-484, SNU-81, and HEK293 cells.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:Direct interactions with Calgranulin B (S100A9) were predicted using STRING analysis, and are indicated by different colored lines: green, red, blue, black, purple, light blue, yellow, sky blue based on the types of evidence for associations.
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List of identified significant genes interacting with Calgranulin B.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:List of identified significant genes interacting with Calgranulin B.
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Cellular components associated with the Calgranulin B-interacting molecules.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:The Calgranulin B-interacting molecules identified in SNU-484 (A), SNU-81 (B), and HEK293 (C) cells were categorized according to cellular component information.
Jae-kyung Myung - One of the best experts on this subject based on the ideXlab platform.
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Identification of Calgranulin B interacting proteins and network analysis in gastrointestinal cancer cells.
PloS one, 2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:Calgranulin B is known to be involved in tumor development, but the underlying molecular mechanism is not clear. To gain insight into possible roles of Calgranulin B, we screened for Calgranulin B-interacting molecules in the SNU-484 gastric cancer and the SNU-81 colon cancer cells. Calgranulin B-interacting partners were identified by yeast two-hybrid and functional information was obtained by computational analysis. Most of the Calgranulin B-interacting partners were involved in metabolic and cellular processes, and found to have molecular function of binding and catalytic activities. Interestingly, 46 molecules in the network of the Calgranulin B-interacting proteins are known to be associated with cancer and FKBP2 was found to interact with Calgranulin B in both SNU-484 and SNU-81 cells. Polyubiquitin-C encoded by UBC, which exhibited an interaction with Calgranulin B, has been associated with various molecules of the extracellular space and plasma membrane identified in our screening, including Na-K-Cl cotransporter 1 and dystonin in SNU-484 cells, and ATPase subunit beta-1 in SNU-81 cells. Our data provide novel insight into the roles of Calgranulin B of gastrointestinal cancer cells, and offer new clues suggesting Calgranulin B acts as an effector molecule through which the cell can communicate with the tumor microenvironment via polyubiquitin-C.
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List of identified significant genes interacting with Calgranulin B.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:List of identified significant genes interacting with Calgranulin B.
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Cellular components associated with the Calgranulin B-interacting molecules.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:The Calgranulin B-interacting molecules identified in SNU-484 (A), SNU-81 (B), and HEK293 (C) cells were categorized according to cellular component information.
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Biological processes overrepresented among the Calgranulin B-interacting partners.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:The distributions of the biological processes represented by the Calgranulin B-interacting molecules identified in SNU-484 (A), SNU-81 (B), and HEK293 (C) cells are shown.
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PANTHER analysis of pathways overrepresented among the Calgranulin B-interacting partners.
2017Co-Authors: Kyung-hee Kim, Byong Chul Yoo, Seung-gu Yeo, Jae-kyung MyungAbstract:The pathway distributions of the Calgranulin B-interacting molecules identified in SNU-484 (A), SNU-81 (B), and HEK293 (C) cells are shown.
