The Experts below are selected from a list of 90603 Experts worldwide ranked by ideXlab platform
Scot C Remick - One of the best experts on this subject based on the ideXlab platform.
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psp94 contributes to chemoresistance and its peptide derivative pck3145 represses tumor growth in ovarian cancer
Oncogene, 2014Co-Authors: J Zhang, Heimo Riedel, Scot C Remick, Michael D Mueller, Jing Jie YuAbstract:Tumor drug resistance remains a major challenge in the treatment of cancer. Here, we show that Prostatic secretory protein 94 (PSP94) levels are reduced in ovarian cancer patients with high levels of excision repair cross-complementing 1 (ERCC1), a marker for chemoresistance. We find that PSP94 is decreased in an ovarian cancer Drug-Resistant Cell Line, and plays an important role in the development of drug resistance in vitro. Our studies indicate that PSP94 can partially reverse drug resistance in mouse tumor models in vivo and that a PSP94 peptide derivative PCK3145 suppresses chemoresistant cancer Cell and tumor growth in vitro and in vivo. Our investigation of the involved molecular mechanisms suggests that PSP94 may confer drug resistance by modulating the Lin28b/Let-7 signaling pathway. We introduce PSP94 and its peptide derivative PCK3145 as potential target to reverse chemoresistance in ovarian cancer and have begun to identify their relevant molecular targets in specific signaling pathways.
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prostasin may contribute to chemoresistance repress cancer Cells in ovarian cancer and is involved in the signaling pathways of casp pak2 p34 actin
Cell Death and Disease, 2014Co-Authors: B X Yan, Michael D Mueller, J Zhang, J X, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
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Prostasin may contribute to chemoresistance, repress cancer Cells in ovarian cancer, and is involved in the signaling pathways of CASP/PAK2-p34/actin.
Cell death & disease, 2014Co-Authors: B X Yan, J Zhang, Michael D Mueller, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
J Zhang - One of the best experts on this subject based on the ideXlab platform.
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psp94 contributes to chemoresistance and its peptide derivative pck3145 represses tumor growth in ovarian cancer
Oncogene, 2014Co-Authors: J Zhang, Heimo Riedel, Scot C Remick, Michael D Mueller, Jing Jie YuAbstract:Tumor drug resistance remains a major challenge in the treatment of cancer. Here, we show that Prostatic secretory protein 94 (PSP94) levels are reduced in ovarian cancer patients with high levels of excision repair cross-complementing 1 (ERCC1), a marker for chemoresistance. We find that PSP94 is decreased in an ovarian cancer Drug-Resistant Cell Line, and plays an important role in the development of drug resistance in vitro. Our studies indicate that PSP94 can partially reverse drug resistance in mouse tumor models in vivo and that a PSP94 peptide derivative PCK3145 suppresses chemoresistant cancer Cell and tumor growth in vitro and in vivo. Our investigation of the involved molecular mechanisms suggests that PSP94 may confer drug resistance by modulating the Lin28b/Let-7 signaling pathway. We introduce PSP94 and its peptide derivative PCK3145 as potential target to reverse chemoresistance in ovarian cancer and have begun to identify their relevant molecular targets in specific signaling pathways.
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prostasin may contribute to chemoresistance repress cancer Cells in ovarian cancer and is involved in the signaling pathways of casp pak2 p34 actin
Cell Death and Disease, 2014Co-Authors: B X Yan, Michael D Mueller, J Zhang, J X, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
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Prostasin may contribute to chemoresistance, repress cancer Cells in ovarian cancer, and is involved in the signaling pathways of CASP/PAK2-p34/actin.
Cell death & disease, 2014Co-Authors: B X Yan, J Zhang, Michael D Mueller, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
B X Yan - One of the best experts on this subject based on the ideXlab platform.
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prostasin may contribute to chemoresistance repress cancer Cells in ovarian cancer and is involved in the signaling pathways of casp pak2 p34 actin
Cell Death and Disease, 2014Co-Authors: B X Yan, Michael D Mueller, J Zhang, J X, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
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Prostasin may contribute to chemoresistance, repress cancer Cells in ovarian cancer, and is involved in the signaling pathways of CASP/PAK2-p34/actin.
Cell death & disease, 2014Co-Authors: B X Yan, J Zhang, Michael D Mueller, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
Michael D Mueller - One of the best experts on this subject based on the ideXlab platform.
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psp94 contributes to chemoresistance and its peptide derivative pck3145 represses tumor growth in ovarian cancer
Oncogene, 2014Co-Authors: J Zhang, Heimo Riedel, Scot C Remick, Michael D Mueller, Jing Jie YuAbstract:Tumor drug resistance remains a major challenge in the treatment of cancer. Here, we show that Prostatic secretory protein 94 (PSP94) levels are reduced in ovarian cancer patients with high levels of excision repair cross-complementing 1 (ERCC1), a marker for chemoresistance. We find that PSP94 is decreased in an ovarian cancer Drug-Resistant Cell Line, and plays an important role in the development of drug resistance in vitro. Our studies indicate that PSP94 can partially reverse drug resistance in mouse tumor models in vivo and that a PSP94 peptide derivative PCK3145 suppresses chemoresistant cancer Cell and tumor growth in vitro and in vivo. Our investigation of the involved molecular mechanisms suggests that PSP94 may confer drug resistance by modulating the Lin28b/Let-7 signaling pathway. We introduce PSP94 and its peptide derivative PCK3145 as potential target to reverse chemoresistance in ovarian cancer and have begun to identify their relevant molecular targets in specific signaling pathways.
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prostasin may contribute to chemoresistance repress cancer Cells in ovarian cancer and is involved in the signaling pathways of casp pak2 p34 actin
Cell Death and Disease, 2014Co-Authors: B X Yan, Michael D Mueller, J Zhang, J X, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
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Prostasin may contribute to chemoresistance, repress cancer Cells in ovarian cancer, and is involved in the signaling pathways of CASP/PAK2-p34/actin.
Cell death & disease, 2014Co-Authors: B X Yan, J Zhang, Michael D Mueller, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
Yi Guo - One of the best experts on this subject based on the ideXlab platform.
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prostasin may contribute to chemoresistance repress cancer Cells in ovarian cancer and is involved in the signaling pathways of casp pak2 p34 actin
Cell Death and Disease, 2014Co-Authors: B X Yan, Michael D Mueller, J Zhang, J X, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
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Prostasin may contribute to chemoresistance, repress cancer Cells in ovarian cancer, and is involved in the signaling pathways of CASP/PAK2-p34/actin.
Cell death & disease, 2014Co-Authors: B X Yan, J Zhang, Michael D Mueller, Yi Guo, Scot C RemickAbstract:Ovarian cancer is the deadliest of gynecologic cancers, largely due to the development of drug resistance in chemotherapy. Prostasin may have an essential role in the oncogenesis. In this study, we show that prostasin is decreased in an ovarian cancer Drug-Resistant Cell Line and in ovarian cancer patients with high levels of excision repair cross-complementing 1, a marker for chemoresistance. Our Cell cultural model investigation demonstrates prostasin has important roles in the development of drug resistance and cancer Cell survival. Forced overexpression of prostasin in ovarian cancer Cells greatly induces Cell death (resulting in 99% Cell death in a Drug-Resistant Cell Line and 100% Cell death in other tested Cell Lines). In addition, the surviving Cells grow at a much lower rate compared with non-overexpressed Cells. In vivo studies indicate that forced overexpression of prostasin in Drug-Resistant Cells greatly inhibits the growth of tumors and may partially reverse drug resistance. Our investigation of the molecular mechanisms suggests that prostasin may repress cancer Cells and/or contribute to chemoresistance by modulating the CASP/P21-activated protein kinase (PAK2)-p34 pathway, and thereafter PAK2-p34/JNK/c-jun and PAK2-p34/mlck/actin signaling pathways. Thus, we introduce prostain as a potential target for treating/repressing some ovarian tumors and have begun to identify their relevant molecular targets in specific signaling pathways.
