High neuropilin and tolloid‐like 1 expression associated with metastasis and poor survival in epithelial ovarian cancer via regulation of actin cytoskeleton
Abnormal expression of neuropilin and tolloid‐like 1 (NETO1) has been detected in some human carcinomas. However, the expression of NETO1 and the underlying mechanism in epithelial ovarian cancer (EOC) remain unknown. In this study, we found that a higher NETO1 expression in EOC tissue samples compa...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-08, Vol.24 (16), p.9114-9124 |
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| creator | Xu, Yunzhao Wang, Wei Chen, Jinling Mao, Haixia Liu, Yuanlin Gu, Shuting Liu, Qinqin Xi, Qinghua Shi, Wenyu |
| description | Abnormal expression of neuropilin and tolloid‐like 1 (NETO1) has been detected in some human carcinomas. However, the expression of NETO1 and the underlying mechanism in epithelial ovarian cancer (EOC) remain unknown. In this study, we found that a higher NETO1 expression in EOC tissue samples compared to normal ovarian tissue samples was significantly correlated with worse overall survival. Additionally, Cox regression analysis suggested that NETO 1 was independently associated with overall survival. NETO1 overexpression enhanced the EOC cells’ migration and invasion capability in vitro via regulation of actin cytoskeleton. Mechanistically, silencing NETO1 reduced the expression of β‐tubulin, F‐actin and KIF2A. In conclusion, our results demonstrated the critical role of NETO1 in EOC invasion, and therapies aimed at inhibiting its expression or activity might significantly control EOC growth, invasion and metastatic dissemination. |
| doi_str_mv | 10.1111/jcmm.15547 |
| format | Article |
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However, the expression of NETO1 and the underlying mechanism in epithelial ovarian cancer (EOC) remain unknown. In this study, we found that a higher NETO1 expression in EOC tissue samples compared to normal ovarian tissue samples was significantly correlated with worse overall survival. Additionally, Cox regression analysis suggested that NETO 1 was independently associated with overall survival. NETO1 overexpression enhanced the EOC cells’ migration and invasion capability in vitro via regulation of actin cytoskeleton. Mechanistically, silencing NETO1 reduced the expression of β‐tubulin, F‐actin and KIF2A. In conclusion, our results demonstrated the critical role of NETO1 in EOC invasion, and therapies aimed at inhibiting its expression or activity might significantly control EOC growth, invasion and metastatic dissemination.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15547</identifier><identifier>PMID: 32638511</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Actin ; actin cytoskeleton ; Actin Cytoskeleton - metabolism ; Actins - metabolism ; Antibodies ; bioinformation ; Carcinoma ; Carcinoma, Ovarian Epithelial - metabolism ; Carcinoma, Ovarian Epithelial - pathology ; Cell Line, Tumor ; Cell migration ; Cell Movement - physiology ; Clinical outcomes ; Cytoskeleton ; epithelial ovarian cancer ; Female ; Gene Expression Regulation, Neoplastic - physiology ; Genes ; Humans ; KIF2A ; Kinesin - metabolism ; Metastases ; Metastasis ; Middle Aged ; NETO1 ; Neuropilin ; Neuropilins - metabolism ; Original ; Ovarian cancer ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Patients ; Proteins ; Receptors, N-Methyl-D-Aspartate - metabolism ; Tubulin ; Tubulin - metabolism</subject><ispartof>Journal of cellular and molecular medicine, 2020-08, Vol.24 (16), p.9114-9124</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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However, the expression of NETO1 and the underlying mechanism in epithelial ovarian cancer (EOC) remain unknown. In this study, we found that a higher NETO1 expression in EOC tissue samples compared to normal ovarian tissue samples was significantly correlated with worse overall survival. Additionally, Cox regression analysis suggested that NETO 1 was independently associated with overall survival. NETO1 overexpression enhanced the EOC cells’ migration and invasion capability in vitro via regulation of actin cytoskeleton. Mechanistically, silencing NETO1 reduced the expression of β‐tubulin, F‐actin and KIF2A. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Yunzhao</au><au>Wang, Wei</au><au>Chen, Jinling</au><au>Mao, Haixia</au><au>Liu, Yuanlin</au><au>Gu, Shuting</au><au>Liu, Qinqin</au><au>Xi, Qinghua</au><au>Shi, Wenyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High neuropilin and tolloid‐like 1 expression associated with metastasis and poor survival in epithelial ovarian cancer via regulation of actin cytoskeleton</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-08</date><risdate>2020</risdate><volume>24</volume><issue>16</issue><spage>9114</spage><epage>9124</epage><pages>9114-9124</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Abnormal expression of neuropilin and tolloid‐like 1 (NETO1) has been detected in some human carcinomas. However, the expression of NETO1 and the underlying mechanism in epithelial ovarian cancer (EOC) remain unknown. In this study, we found that a higher NETO1 expression in EOC tissue samples compared to normal ovarian tissue samples was significantly correlated with worse overall survival. Additionally, Cox regression analysis suggested that NETO 1 was independently associated with overall survival. NETO1 overexpression enhanced the EOC cells’ migration and invasion capability in vitro via regulation of actin cytoskeleton. Mechanistically, silencing NETO1 reduced the expression of β‐tubulin, F‐actin and KIF2A. In conclusion, our results demonstrated the critical role of NETO1 in EOC invasion, and therapies aimed at inhibiting its expression or activity might significantly control EOC growth, invasion and metastatic dissemination.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32638511</pmid><doi>10.1111/jcmm.15547</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-4279-2213</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Actin actin cytoskeleton Actin Cytoskeleton - metabolism Actins - metabolism Antibodies bioinformation Carcinoma Carcinoma, Ovarian Epithelial - metabolism Carcinoma, Ovarian Epithelial - pathology Cell Line, Tumor Cell migration Cell Movement - physiology Clinical outcomes Cytoskeleton epithelial ovarian cancer Female Gene Expression Regulation, Neoplastic - physiology Genes Humans KIF2A Kinesin - metabolism Metastases Metastasis Middle Aged NETO1 Neuropilin Neuropilins - metabolism Original Ovarian cancer Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Patients Proteins Receptors, N-Methyl-D-Aspartate - metabolism Tubulin Tubulin - metabolism |
| title | High neuropilin and tolloid‐like 1 expression associated with metastasis and poor survival in epithelial ovarian cancer via regulation of actin cytoskeleton |
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