author_facet Wang, Guosen
Sheng, Weiwei
Tang, Jingtong
Li, Xin
Zhou, Jianping
Dong, Ming
Wang, Guosen
Sheng, Weiwei
Tang, Jingtong
Li, Xin
Zhou, Jianping
Dong, Ming
author Wang, Guosen
Sheng, Weiwei
Tang, Jingtong
Li, Xin
Zhou, Jianping
Dong, Ming
spellingShingle Wang, Guosen
Sheng, Weiwei
Tang, Jingtong
Li, Xin
Zhou, Jianping
Dong, Ming
Bioscience Reports
Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
Cell Biology
Molecular Biology
Biochemistry
Biophysics
author_sort wang, guosen
spelling Wang, Guosen Sheng, Weiwei Tang, Jingtong Li, Xin Zhou, Jianping Dong, Ming 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20191488 <jats:title>Abstract</jats:title> <jats:p>Serine-arginine protein kinase 2 (SRPK2) is aberrantly expressed in human malignancies including colorectal cancer (CRC). However, little is known about the molecular mechanisms, and the role of SRPK2 in chemosensitivity remains unexplored in CRC. We recently showed that SRPK2 promotes pancreatic cancer progression by down-regulating Numb and p53. Therefore, we investigated the cooperation between SRPK2, Numb and p53 in the cell migration, invasion and chemosensitivity of CRC in vitro. Here, we showed that SRPK2 expression was higher in CRC tumors than in nontumor tissues. SRPK2 expression was positively associated with clinicopathological characteristics of CRC patients, including tumor differentiation, T stage, N stage and UICC stage. Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex with or without the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the up-regulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. These results thus reveal a novel role of SRPK2-Numb-p53 signaling in the progression of CRC and demonstrate that SRPK2 is a potential therapeutic target for CRC clinical therapy.</jats:p> Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer Bioscience Reports
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title Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_unstemmed Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_full Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_fullStr Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_full_unstemmed Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_short Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_sort cooperation of srpk2, numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
topic Cell Biology
Molecular Biology
Biochemistry
Biophysics
url http://dx.doi.org/10.1042/bsr20191488
publishDate 2020
physical
description <jats:title>Abstract</jats:title> <jats:p>Serine-arginine protein kinase 2 (SRPK2) is aberrantly expressed in human malignancies including colorectal cancer (CRC). However, little is known about the molecular mechanisms, and the role of SRPK2 in chemosensitivity remains unexplored in CRC. We recently showed that SRPK2 promotes pancreatic cancer progression by down-regulating Numb and p53. Therefore, we investigated the cooperation between SRPK2, Numb and p53 in the cell migration, invasion and chemosensitivity of CRC in vitro. Here, we showed that SRPK2 expression was higher in CRC tumors than in nontumor tissues. SRPK2 expression was positively associated with clinicopathological characteristics of CRC patients, including tumor differentiation, T stage, N stage and UICC stage. Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex with or without the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the up-regulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. These results thus reveal a novel role of SRPK2-Numb-p53 signaling in the progression of CRC and demonstrate that SRPK2 is a potential therapeutic target for CRC clinical therapy.</jats:p>
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author Wang, Guosen, Sheng, Weiwei, Tang, Jingtong, Li, Xin, Zhou, Jianping, Dong, Ming
author_facet Wang, Guosen, Sheng, Weiwei, Tang, Jingtong, Li, Xin, Zhou, Jianping, Dong, Ming, Wang, Guosen, Sheng, Weiwei, Tang, Jingtong, Li, Xin, Zhou, Jianping, Dong, Ming
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description <jats:title>Abstract</jats:title> <jats:p>Serine-arginine protein kinase 2 (SRPK2) is aberrantly expressed in human malignancies including colorectal cancer (CRC). However, little is known about the molecular mechanisms, and the role of SRPK2 in chemosensitivity remains unexplored in CRC. We recently showed that SRPK2 promotes pancreatic cancer progression by down-regulating Numb and p53. Therefore, we investigated the cooperation between SRPK2, Numb and p53 in the cell migration, invasion and chemosensitivity of CRC in vitro. Here, we showed that SRPK2 expression was higher in CRC tumors than in nontumor tissues. SRPK2 expression was positively associated with clinicopathological characteristics of CRC patients, including tumor differentiation, T stage, N stage and UICC stage. Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex with or without the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the up-regulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. These results thus reveal a novel role of SRPK2-Numb-p53 signaling in the progression of CRC and demonstrate that SRPK2 is a potential therapeutic target for CRC clinical therapy.</jats:p>
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spelling Wang, Guosen Sheng, Weiwei Tang, Jingtong Li, Xin Zhou, Jianping Dong, Ming 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20191488 <jats:title>Abstract</jats:title> <jats:p>Serine-arginine protein kinase 2 (SRPK2) is aberrantly expressed in human malignancies including colorectal cancer (CRC). However, little is known about the molecular mechanisms, and the role of SRPK2 in chemosensitivity remains unexplored in CRC. We recently showed that SRPK2 promotes pancreatic cancer progression by down-regulating Numb and p53. Therefore, we investigated the cooperation between SRPK2, Numb and p53 in the cell migration, invasion and chemosensitivity of CRC in vitro. Here, we showed that SRPK2 expression was higher in CRC tumors than in nontumor tissues. SRPK2 expression was positively associated with clinicopathological characteristics of CRC patients, including tumor differentiation, T stage, N stage and UICC stage. Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex with or without the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the up-regulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. These results thus reveal a novel role of SRPK2-Numb-p53 signaling in the progression of CRC and demonstrate that SRPK2 is a potential therapeutic target for CRC clinical therapy.</jats:p> Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer Bioscience Reports
spellingShingle Wang, Guosen, Sheng, Weiwei, Tang, Jingtong, Li, Xin, Zhou, Jianping, Dong, Ming, Bioscience Reports, Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer, Cell Biology, Molecular Biology, Biochemistry, Biophysics
title Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_full Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_fullStr Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_full_unstemmed Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_short Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_sort cooperation of srpk2, numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
title_unstemmed Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer
topic Cell Biology, Molecular Biology, Biochemistry, Biophysics
url http://dx.doi.org/10.1042/bsr20191488