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Sung-dae Cho - One of the best experts on this subject based on the ideXlab platform.
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Silymarin and its active component silibinin act as novel therapeutic alternatives for Salivary Gland Cancer by targeting the ERK1/2-Bim signaling cascade
Cellular Oncology, 2017Co-Authors: Eun-sun Choi, Jiae Shin, Inhyoung Yang, Boonsil Jang, Nam-pyo Cho, Dong-hoon Won, Hye-jeong Kwon, Seong Doo Hong, Sung-dae ChoAbstract:Purpose Approximately 20% of all Salivary Gland Cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of Salivary Gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin. Methods The effects of silymarin and its active component silibinin on Salivary Gland Cancer-derived MC3 and HN22 cells and their underlying molecular mechanisms were examined using trypan blue exclusion, 4′-6-diamidino-2-phenylindole (DAPI) staining, Live/Dead, Annexin V/PI staining, mitochondrial membrane potential (ΔΨm) measurement, quantitative RT-PCR, soft agar colony formation and Western blotting analyses. Results We found that silymarin and silibinin dramatically increased the expression of the pro-apoptotic protein Bim in a concentration- and time-dependent manner and, concomitantly, induced apoptosis in MC3 and HN22 cells. We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway. Conclusions Taken together, we conclude that ERK1/2 signaling pathway inhibition by silymarin and silibinin increases the expression of the pro-apoptotic Bcl-2 family member Bim which, subsequently, induces mitochondria-mediated apoptosis in Salivary Gland Cancer-derived cells.
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silymarin and its active component silibinin act as novel therapeutic alternatives for Salivary Gland Cancer by targeting the erk1 2 bim signaling cascade
Cellular Oncology, 2017Co-Authors: Eun-sun Choi, Jiae Shin, Inhyoung Yang, Boonsil Jang, Nam-pyo Cho, Dong-hoon Won, Hye-jeong Kwon, Seong Doo Hong, Sung-dae ChoAbstract:Purpose Approximately 20% of all Salivary Gland Cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of Salivary Gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin.
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Convallaria keiskei as a novel therapeutic alternative for Salivary Gland Cancer treatment by targeting myeloid cell leukemia-1.
Head & neck, 2015Co-Authors: Haeng-eun Lee, Jiae Shin, Insun Hong, Inhyoung Yang, Jeong-seok Nam, Myung-jo You, Sung-dae ChoAbstract:Various chemotherapeutic agents have been used largely for the treatment of Salivary Gland Cancer. However, results are disappointing, and these agents can cause some serious side effects. Therefore, recent studies have focused on the possible roles of natural products to overcome these limitations. Salivary Gland Cancer cells treated with or without Convallaria keiskei (MECK) for 24 hours. Apoptotic changes were evaluated by live/dead assay, immunoblotting, and expression levels of caspase-3 and B-cell lymphoma-2 family member. MECK significantly inhibited Salivary Gland Cancer growth. At the molecular level, MECK dramatically reduced myeloid cell leukemia-1 (Mcl-1) in a translation-dependent manner and thereby induced apoptosis through Bax/Bid. Furthermore, we found that Mcl-1 could be a potential therapeutic target of MECK-induced apoptosis and its stability is regulated by extracellular signal-regulated kinases 1/2 (ERK1/2) signaling MECK can be used as a safe and efficient therapeutic alternative for the treatment of Salivary Gland Cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E761-E770, 2016. © 2015 Wiley Periodicals, Inc.
Inhyoung Yang - One of the best experts on this subject based on the ideXlab platform.
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Silymarin and its active component silibinin act as novel therapeutic alternatives for Salivary Gland Cancer by targeting the ERK1/2-Bim signaling cascade
Cellular Oncology, 2017Co-Authors: Eun-sun Choi, Jiae Shin, Inhyoung Yang, Boonsil Jang, Nam-pyo Cho, Dong-hoon Won, Hye-jeong Kwon, Seong Doo Hong, Sung-dae ChoAbstract:Purpose Approximately 20% of all Salivary Gland Cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of Salivary Gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin. Methods The effects of silymarin and its active component silibinin on Salivary Gland Cancer-derived MC3 and HN22 cells and their underlying molecular mechanisms were examined using trypan blue exclusion, 4′-6-diamidino-2-phenylindole (DAPI) staining, Live/Dead, Annexin V/PI staining, mitochondrial membrane potential (ΔΨm) measurement, quantitative RT-PCR, soft agar colony formation and Western blotting analyses. Results We found that silymarin and silibinin dramatically increased the expression of the pro-apoptotic protein Bim in a concentration- and time-dependent manner and, concomitantly, induced apoptosis in MC3 and HN22 cells. We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway. Conclusions Taken together, we conclude that ERK1/2 signaling pathway inhibition by silymarin and silibinin increases the expression of the pro-apoptotic Bcl-2 family member Bim which, subsequently, induces mitochondria-mediated apoptosis in Salivary Gland Cancer-derived cells.
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silymarin and its active component silibinin act as novel therapeutic alternatives for Salivary Gland Cancer by targeting the erk1 2 bim signaling cascade
Cellular Oncology, 2017Co-Authors: Eun-sun Choi, Jiae Shin, Inhyoung Yang, Boonsil Jang, Nam-pyo Cho, Dong-hoon Won, Hye-jeong Kwon, Seong Doo Hong, Sung-dae ChoAbstract:Purpose Approximately 20% of all Salivary Gland Cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of Salivary Gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin.
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convallaria keiskei as a novel therapeutic alternative for Salivary Gland Cancer treatment by targeting myeloid cell leukemia 1
Head and Neck-journal for The Sciences and Specialties of The Head and Neck, 2016Co-Authors: Jiae Shin, Insun Hong, Inhyoung YangAbstract:Background Various chemotherapeutic agents have been used largely for the treatment of Salivary Gland Cancer. However, results are disappointing, and these agents can cause some serious side effects. Therefore, recent studies have focused on the possible roles of natural products to overcome these limitations. Methods Salivary Gland Cancer cells treated with or without Convallaria keiskei (MECK) for 24 hours. Apoptotic changes were evaluated by live/dead assay, immunoblotting, and expression levels of caspase-3 and B-cell lymphoma-2 family member. Results MECK significantly inhibited Salivary Gland Cancer growth. At the molecular level, MECK dramatically reduced myeloid cell leukemia-1 (Mcl-1) in a translation-dependent manner and thereby induced apoptosis through Bax/Bid. Furthermore, we found that Mcl-1 could be a potential therapeutic target of MECK-induced apoptosis and its stability is regulated by extracellular signal-regulated kinases 1/2 (ERK1/2) signaling Conclusion MECK can be used as a safe and efficient therapeutic alternative for the treatment of Salivary Gland Cancer. © 2015 Wiley Periodicals, Inc. Head Neck, 2015
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Convallaria keiskei as a novel therapeutic alternative for Salivary Gland Cancer treatment by targeting myeloid cell leukemia-1.
Head & neck, 2015Co-Authors: Haeng-eun Lee, Jiae Shin, Insun Hong, Inhyoung Yang, Jeong-seok Nam, Myung-jo You, Sung-dae ChoAbstract:Various chemotherapeutic agents have been used largely for the treatment of Salivary Gland Cancer. However, results are disappointing, and these agents can cause some serious side effects. Therefore, recent studies have focused on the possible roles of natural products to overcome these limitations. Salivary Gland Cancer cells treated with or without Convallaria keiskei (MECK) for 24 hours. Apoptotic changes were evaluated by live/dead assay, immunoblotting, and expression levels of caspase-3 and B-cell lymphoma-2 family member. MECK significantly inhibited Salivary Gland Cancer growth. At the molecular level, MECK dramatically reduced myeloid cell leukemia-1 (Mcl-1) in a translation-dependent manner and thereby induced apoptosis through Bax/Bid. Furthermore, we found that Mcl-1 could be a potential therapeutic target of MECK-induced apoptosis and its stability is regulated by extracellular signal-regulated kinases 1/2 (ERK1/2) signaling MECK can be used as a safe and efficient therapeutic alternative for the treatment of Salivary Gland Cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E761-E770, 2016. © 2015 Wiley Periodicals, Inc.
Jiae Shin - One of the best experts on this subject based on the ideXlab platform.
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Silymarin and its active component silibinin act as novel therapeutic alternatives for Salivary Gland Cancer by targeting the ERK1/2-Bim signaling cascade
Cellular Oncology, 2017Co-Authors: Eun-sun Choi, Jiae Shin, Inhyoung Yang, Boonsil Jang, Nam-pyo Cho, Dong-hoon Won, Hye-jeong Kwon, Seong Doo Hong, Sung-dae ChoAbstract:Purpose Approximately 20% of all Salivary Gland Cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of Salivary Gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin. Methods The effects of silymarin and its active component silibinin on Salivary Gland Cancer-derived MC3 and HN22 cells and their underlying molecular mechanisms were examined using trypan blue exclusion, 4′-6-diamidino-2-phenylindole (DAPI) staining, Live/Dead, Annexin V/PI staining, mitochondrial membrane potential (ΔΨm) measurement, quantitative RT-PCR, soft agar colony formation and Western blotting analyses. Results We found that silymarin and silibinin dramatically increased the expression of the pro-apoptotic protein Bim in a concentration- and time-dependent manner and, concomitantly, induced apoptosis in MC3 and HN22 cells. We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway. Conclusions Taken together, we conclude that ERK1/2 signaling pathway inhibition by silymarin and silibinin increases the expression of the pro-apoptotic Bcl-2 family member Bim which, subsequently, induces mitochondria-mediated apoptosis in Salivary Gland Cancer-derived cells.
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silymarin and its active component silibinin act as novel therapeutic alternatives for Salivary Gland Cancer by targeting the erk1 2 bim signaling cascade
Cellular Oncology, 2017Co-Authors: Eun-sun Choi, Jiae Shin, Inhyoung Yang, Boonsil Jang, Nam-pyo Cho, Dong-hoon Won, Hye-jeong Kwon, Seong Doo Hong, Sung-dae ChoAbstract:Purpose Approximately 20% of all Salivary Gland Cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of Salivary Gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin.
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convallaria keiskei as a novel therapeutic alternative for Salivary Gland Cancer treatment by targeting myeloid cell leukemia 1
Head and Neck-journal for The Sciences and Specialties of The Head and Neck, 2016Co-Authors: Jiae Shin, Insun Hong, Inhyoung YangAbstract:Background Various chemotherapeutic agents have been used largely for the treatment of Salivary Gland Cancer. However, results are disappointing, and these agents can cause some serious side effects. Therefore, recent studies have focused on the possible roles of natural products to overcome these limitations. Methods Salivary Gland Cancer cells treated with or without Convallaria keiskei (MECK) for 24 hours. Apoptotic changes were evaluated by live/dead assay, immunoblotting, and expression levels of caspase-3 and B-cell lymphoma-2 family member. Results MECK significantly inhibited Salivary Gland Cancer growth. At the molecular level, MECK dramatically reduced myeloid cell leukemia-1 (Mcl-1) in a translation-dependent manner and thereby induced apoptosis through Bax/Bid. Furthermore, we found that Mcl-1 could be a potential therapeutic target of MECK-induced apoptosis and its stability is regulated by extracellular signal-regulated kinases 1/2 (ERK1/2) signaling Conclusion MECK can be used as a safe and efficient therapeutic alternative for the treatment of Salivary Gland Cancer. © 2015 Wiley Periodicals, Inc. Head Neck, 2015
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Convallaria keiskei as a novel therapeutic alternative for Salivary Gland Cancer treatment by targeting myeloid cell leukemia-1.
Head & neck, 2015Co-Authors: Haeng-eun Lee, Jiae Shin, Insun Hong, Inhyoung Yang, Jeong-seok Nam, Myung-jo You, Sung-dae ChoAbstract:Various chemotherapeutic agents have been used largely for the treatment of Salivary Gland Cancer. However, results are disappointing, and these agents can cause some serious side effects. Therefore, recent studies have focused on the possible roles of natural products to overcome these limitations. Salivary Gland Cancer cells treated with or without Convallaria keiskei (MECK) for 24 hours. Apoptotic changes were evaluated by live/dead assay, immunoblotting, and expression levels of caspase-3 and B-cell lymphoma-2 family member. MECK significantly inhibited Salivary Gland Cancer growth. At the molecular level, MECK dramatically reduced myeloid cell leukemia-1 (Mcl-1) in a translation-dependent manner and thereby induced apoptosis through Bax/Bid. Furthermore, we found that Mcl-1 could be a potential therapeutic target of MECK-induced apoptosis and its stability is regulated by extracellular signal-regulated kinases 1/2 (ERK1/2) signaling MECK can be used as a safe and efficient therapeutic alternative for the treatment of Salivary Gland Cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E761-E770, 2016. © 2015 Wiley Periodicals, Inc.
Markus Stenner - One of the best experts on this subject based on the ideXlab platform.
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Stromal collagen type VI associates with features of malignancy and predicts poor prognosis in Salivary Gland Cancer
Cellular Oncology, 2018Co-Authors: Linus Angenendt, Jan-henrik Mikesch, Dennis Görlich, Alina Busch, Irina Arnhold, Claudia Rudack, Wolfgang Hartmann, Eva Wardelmann, Wolfgang E. Berdel, Markus StennerAbstract:Purpose Collagen Type VI (COLVI) is an extracellular matrix protein that is upregulated in various solid tumours during tumour progression and has been shown to stimulate proliferation, suppress apoptosis and promote invasion and metastasis. It has also been described as a mediator of chemotherapy resistance and as a therapeutic target in preclinical Cancer models. Here, we aimed to analyse the prognostic role of COLVI in Salivary Gland Cancer (SGC). Methods Stromal COLVI protein expression was assessed in primary SGC specimens of 91 patients using immunohistochemistry (IHC). The IHC expression patterns obtained were subsequently correlated with various survival and clinicopathological features, including Ki-67 and p53 expression. Results We found that COLVI was expressed in all SGC specimens. High expression was found to be associated with features of malignancy such as high histologic grades, advanced and invasive T stages and metastatic lymph node involvement ( p
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Stromal collagen type VI associates with features of malignancy and predicts poor prognosis in Salivary Gland Cancer.
Cellular oncology (Dordrecht), 2018Co-Authors: Linus Angenendt, Jan-henrik Mikesch, Dennis Görlich, Alina Busch, Irina Arnhold, Claudia Rudack, Wolfgang Hartmann, Eva Wardelmann, Wolfgang E. Berdel, Markus StennerAbstract:Purpose Collagen Type VI (COLVI) is an extracellular matrix protein that is upregulated in various solid tumours during tumour progression and has been shown to stimulate proliferation, suppress apoptosis and promote invasion and metastasis. It has also been described as a mediator of chemotherapy resistance and as a therapeutic target in preclinical Cancer models. Here, we aimed to analyse the prognostic role of COLVI in Salivary Gland Cancer (SGC).
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AAA+ ATPases Reptin and Pontin as potential diagnostic and prognostic biomarkers in Salivary Gland Cancer - a short report
Cellular oncology (Dordrecht), 2018Co-Authors: Jan-henrik Mikesch, Linus Angenendt, Claudia Rudack, Wolfgang Hartmann, Eva Wardelmann, Wolfgang E. Berdel, Otmar Huber, Christoph Schliemann, Maria Francisca Arteaga, Markus StennerAbstract:Purpose Salivary Gland Cancer (SGC) is a rare and heterogeneous disease with significant differences in recurrence and metastasis characteristics. As yet, little is known about the mechanisms underlying the initiation and/or progression of these diverse tumors. In recent years, the AAA+ ATPase family members Pontin (RuvBL1, Tip49a) and Reptin (RuvBL2, Tip49b) have been implicated in various processes, including transcription regulation, chromatin remodeling and DNA damage repair, that are frequently deregulated in Cancer. The aim of this study was to assess the clinical and functional significance of Reptin and Pontin expression in SGC.
Linus Angenendt - One of the best experts on this subject based on the ideXlab platform.
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Stromal collagen type VI associates with features of malignancy and predicts poor prognosis in Salivary Gland Cancer
Cellular Oncology, 2018Co-Authors: Linus Angenendt, Jan-henrik Mikesch, Dennis Görlich, Alina Busch, Irina Arnhold, Claudia Rudack, Wolfgang Hartmann, Eva Wardelmann, Wolfgang E. Berdel, Markus StennerAbstract:Purpose Collagen Type VI (COLVI) is an extracellular matrix protein that is upregulated in various solid tumours during tumour progression and has been shown to stimulate proliferation, suppress apoptosis and promote invasion and metastasis. It has also been described as a mediator of chemotherapy resistance and as a therapeutic target in preclinical Cancer models. Here, we aimed to analyse the prognostic role of COLVI in Salivary Gland Cancer (SGC). Methods Stromal COLVI protein expression was assessed in primary SGC specimens of 91 patients using immunohistochemistry (IHC). The IHC expression patterns obtained were subsequently correlated with various survival and clinicopathological features, including Ki-67 and p53 expression. Results We found that COLVI was expressed in all SGC specimens. High expression was found to be associated with features of malignancy such as high histologic grades, advanced and invasive T stages and metastatic lymph node involvement ( p
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Stromal collagen type VI associates with features of malignancy and predicts poor prognosis in Salivary Gland Cancer.
Cellular oncology (Dordrecht), 2018Co-Authors: Linus Angenendt, Jan-henrik Mikesch, Dennis Görlich, Alina Busch, Irina Arnhold, Claudia Rudack, Wolfgang Hartmann, Eva Wardelmann, Wolfgang E. Berdel, Markus StennerAbstract:Purpose Collagen Type VI (COLVI) is an extracellular matrix protein that is upregulated in various solid tumours during tumour progression and has been shown to stimulate proliferation, suppress apoptosis and promote invasion and metastasis. It has also been described as a mediator of chemotherapy resistance and as a therapeutic target in preclinical Cancer models. Here, we aimed to analyse the prognostic role of COLVI in Salivary Gland Cancer (SGC).
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AAA+ ATPases Reptin and Pontin as potential diagnostic and prognostic biomarkers in Salivary Gland Cancer - a short report
Cellular oncology (Dordrecht), 2018Co-Authors: Jan-henrik Mikesch, Linus Angenendt, Claudia Rudack, Wolfgang Hartmann, Eva Wardelmann, Wolfgang E. Berdel, Otmar Huber, Christoph Schliemann, Maria Francisca Arteaga, Markus StennerAbstract:Purpose Salivary Gland Cancer (SGC) is a rare and heterogeneous disease with significant differences in recurrence and metastasis characteristics. As yet, little is known about the mechanisms underlying the initiation and/or progression of these diverse tumors. In recent years, the AAA+ ATPase family members Pontin (RuvBL1, Tip49a) and Reptin (RuvBL2, Tip49b) have been implicated in various processes, including transcription regulation, chromatin remodeling and DNA damage repair, that are frequently deregulated in Cancer. The aim of this study was to assess the clinical and functional significance of Reptin and Pontin expression in SGC.
