SKA1 regulates actin cytoskeleton remodelling via activating Cdc42 and influences the migration of pancreatic ductal adenocarcinoma cells
Objectives Spindle and kinetochore–associated protein 1(SKA1), originally identified as a protein essential for proper chromosome segregation, has been recently linked to multiple malignancies. This study aimed to explore the biological, clinical role and molecular mechanism of SKA1 in pancreatic ca...
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| Veröffentlicht in: | Cell proliferation 2020-04, Vol.53 (4), p.e12799-n/a |
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| creator | Li, Tong Liu, Xu Xu, Bin Wu, Wei Zang, Yi Li, Juanjuan Wei, Lumin Qian, Yuting Xu, Hui Xie, Mingping Wang, Qi Wang, Lifu |
| description | Objectives
Spindle and kinetochore–associated protein 1(SKA1), originally identified as a protein essential for proper chromosome segregation, has been recently linked to multiple malignancies. This study aimed to explore the biological, clinical role and molecular mechanism of SKA1 in pancreatic carcinogenesis.
Materials and Methods
SKA1 expression was detected in 145 pancreatic ductal adenocarcinoma (PDAC) specimens by immunohistochemistry. Biological behaviour assays were used to determine the role of SKA1 in PDAC progression in vitro and in vivo. Using isobaric tags for relative and absolute quantitation (iTRAQ), SKA1’s downstream proteins were examined. Moreover, cytochalasin B and ZCL278 were used to explore the changes of SKA1‐induced signalling and cell morphology, with further confirmation by immunoblotting and immunofluorescence assays.
Results
Increased SKA1 expression was significantly correlated with tumour size and cellular differentiation degree in PDAC tissues. Furthermore, elevated levels of SKA1 reflected shorter overall survival (P = .019). As for biological behaviour, SKA1 acted as a tumour promotor in PDAC, overexpression of SKA1 facilitates cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, we demonstrated that SKA1 enhanced pancreatic cancer aggressiveness by inhibiting G2/M arrest and regulating actin cytoskeleton organization via activating Cdc42.
Conclusions
This study revealed novel roles for SKA1 as an important regulator of actin cytoskeleton organization and an oncogene in PDAC cells, which may provide insights into developing novel therapeutics. |
| doi_str_mv | 10.1111/cpr.12799 |
| format | Article |
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Spindle and kinetochore–associated protein 1(SKA1), originally identified as a protein essential for proper chromosome segregation, has been recently linked to multiple malignancies. This study aimed to explore the biological, clinical role and molecular mechanism of SKA1 in pancreatic carcinogenesis.
Materials and Methods
SKA1 expression was detected in 145 pancreatic ductal adenocarcinoma (PDAC) specimens by immunohistochemistry. Biological behaviour assays were used to determine the role of SKA1 in PDAC progression in vitro and in vivo. Using isobaric tags for relative and absolute quantitation (iTRAQ), SKA1’s downstream proteins were examined. Moreover, cytochalasin B and ZCL278 were used to explore the changes of SKA1‐induced signalling and cell morphology, with further confirmation by immunoblotting and immunofluorescence assays.
Results
Increased SKA1 expression was significantly correlated with tumour size and cellular differentiation degree in PDAC tissues. Furthermore, elevated levels of SKA1 reflected shorter overall survival (P = .019). As for biological behaviour, SKA1 acted as a tumour promotor in PDAC, overexpression of SKA1 facilitates cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, we demonstrated that SKA1 enhanced pancreatic cancer aggressiveness by inhibiting G2/M arrest and regulating actin cytoskeleton organization via activating Cdc42.
Conclusions
This study revealed novel roles for SKA1 as an important regulator of actin cytoskeleton organization and an oncogene in PDAC cells, which may provide insights into developing novel therapeutics.</description><identifier>ISSN: 0960-7722</identifier><identifier>EISSN: 1365-2184</identifier><identifier>DOI: 10.1111/cpr.12799</identifier><identifier>PMID: 32232899</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Actin ; Actin Cytoskeleton - metabolism ; Actin Cytoskeleton - pathology ; Adenocarcinoma ; Aged ; Cancer therapies ; Carcinogenesis ; Carcinogens ; Carcinoma, Pancreatic Ductal - metabolism ; Carcinoma, Pancreatic Ductal - pathology ; cdc42 GTP-Binding Protein - analysis ; cdc42 GTP-Binding Protein - metabolism ; Cdc42 protein ; Cell adhesion & migration ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell morphology ; Cell Movement ; Cell Proliferation ; Chromosomal Proteins, Non-Histone - analysis ; Chromosomal Proteins, Non-Histone - metabolism ; Chromosomes ; Cytochalasin B ; Cytology ; Cytoskeleton ; Differentiation (biology) ; Female ; G2 Phase Cell Cycle Checkpoints ; Gene expression ; Humans ; Immunoblotting ; Immunofluorescence ; Immunohistochemistry ; Male ; Metastasis ; Middle Aged ; Morphology ; Neoplasm Invasiveness - pathology ; Original ; Pancreatic cancer ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Proteins ; Quantitation ; Tumors</subject><ispartof>Cell proliferation, 2020-04, Vol.53 (4), p.e12799-n/a</ispartof><rights>2020 The Authors. Published by John Wiley & Sons Ltd.</rights><rights>2020 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4719-610a1c204bb46583ef9d07101d6e12a9262342a9f6de38b2ae8f50157ba0f52e3</citedby><cites>FETCH-LOGICAL-c4719-610a1c204bb46583ef9d07101d6e12a9262342a9f6de38b2ae8f50157ba0f52e3</cites><orcidid>0000-0001-5172-9932</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162805/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162805/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32232899$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Tong</creatorcontrib><creatorcontrib>Liu, Xu</creatorcontrib><creatorcontrib>Xu, Bin</creatorcontrib><creatorcontrib>Wu, Wei</creatorcontrib><creatorcontrib>Zang, Yi</creatorcontrib><creatorcontrib>Li, Juanjuan</creatorcontrib><creatorcontrib>Wei, Lumin</creatorcontrib><creatorcontrib>Qian, Yuting</creatorcontrib><creatorcontrib>Xu, Hui</creatorcontrib><creatorcontrib>Xie, Mingping</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Wang, Lifu</creatorcontrib><title>SKA1 regulates actin cytoskeleton remodelling via activating Cdc42 and influences the migration of pancreatic ductal adenocarcinoma cells</title><title>Cell proliferation</title><addtitle>Cell Prolif</addtitle><description>Objectives
Spindle and kinetochore–associated protein 1(SKA1), originally identified as a protein essential for proper chromosome segregation, has been recently linked to multiple malignancies. This study aimed to explore the biological, clinical role and molecular mechanism of SKA1 in pancreatic carcinogenesis.
Materials and Methods
SKA1 expression was detected in 145 pancreatic ductal adenocarcinoma (PDAC) specimens by immunohistochemistry. Biological behaviour assays were used to determine the role of SKA1 in PDAC progression in vitro and in vivo. Using isobaric tags for relative and absolute quantitation (iTRAQ), SKA1’s downstream proteins were examined. Moreover, cytochalasin B and ZCL278 were used to explore the changes of SKA1‐induced signalling and cell morphology, with further confirmation by immunoblotting and immunofluorescence assays.
Results
Increased SKA1 expression was significantly correlated with tumour size and cellular differentiation degree in PDAC tissues. Furthermore, elevated levels of SKA1 reflected shorter overall survival (P = .019). As for biological behaviour, SKA1 acted as a tumour promotor in PDAC, overexpression of SKA1 facilitates cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, we demonstrated that SKA1 enhanced pancreatic cancer aggressiveness by inhibiting G2/M arrest and regulating actin cytoskeleton organization via activating Cdc42.
Conclusions
This study revealed novel roles for SKA1 as an important regulator of actin cytoskeleton organization and an oncogene in PDAC cells, which may provide insights into developing novel therapeutics.</description><subject>Actin</subject><subject>Actin Cytoskeleton - metabolism</subject><subject>Actin Cytoskeleton - pathology</subject><subject>Adenocarcinoma</subject><subject>Aged</subject><subject>Cancer therapies</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>cdc42 GTP-Binding Protein - analysis</subject><subject>cdc42 GTP-Binding Protein - metabolism</subject><subject>Cdc42 protein</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell morphology</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Chromosomal Proteins, Non-Histone - analysis</subject><subject>Chromosomal Proteins, Non-Histone - metabolism</subject><subject>Chromosomes</subject><subject>Cytochalasin B</subject><subject>Cytology</subject><subject>Cytoskeleton</subject><subject>Differentiation (biology)</subject><subject>Female</subject><subject>G2 Phase Cell Cycle Checkpoints</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Morphology</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Original</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Proteins</subject><subject>Quantitation</subject><subject>Tumors</subject><issn>0960-7722</issn><issn>1365-2184</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kktv1DAQgC0EotvCgT-ALHGhh7R-JH5ckKoVLYhKIB5ny3EmW5fEXuxk0f6E_ut6u6UCJPBlNJrP33jkQegFJSe0nFO3TieUSa0foQXloqkYVfVjtCBakEpKxg7QYc7XhFBOpXiKDjhjnCmtF-jmy4czihOs5sFOkLF1kw_YbaeYv8MAUwylOMYOhsGHFd54e4ds7LRLl52rGbahwz70wwzBFcV0BXj0q1SQcjv2eG2DS1BSh7vZTXbAtoMQnU3Ohzha7Io9P0NPejtkeH4fj9C387dfl--qy48X75dnl5WrJdWVoMRSx0jdtrVoFIded0RSQjsBlFnNBON1ib3ogKuWWVB9Q2gjW0v6hgE_Qm_23vXcjtA5CFOyg1knP9q0NdF682cl-CuzihsjqWCKNEXw-l6Q4o8Z8mRGn3cj2ABxzoZx1TDJSs-CvvoLvY5zCmU8wxoitFBKqv9SXBPONW12ruM95VLMOUH_8GRKzG4NTFkDc7cGhX35-4wP5K9_L8DpHvjpB9j-22SWnz7vlbd0p725</recordid><startdate>202004</startdate><enddate>202004</enddate><creator>Li, Tong</creator><creator>Liu, Xu</creator><creator>Xu, Bin</creator><creator>Wu, Wei</creator><creator>Zang, Yi</creator><creator>Li, Juanjuan</creator><creator>Wei, Lumin</creator><creator>Qian, Yuting</creator><creator>Xu, Hui</creator><creator>Xie, Mingping</creator><creator>Wang, Qi</creator><creator>Wang, Lifu</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5172-9932</orcidid></search><sort><creationdate>202004</creationdate><title>SKA1 regulates actin cytoskeleton remodelling via activating Cdc42 and influences the migration of pancreatic ductal adenocarcinoma cells</title><author>Li, Tong ; Liu, Xu ; Xu, Bin ; Wu, Wei ; Zang, Yi ; Li, Juanjuan ; Wei, Lumin ; Qian, Yuting ; Xu, Hui ; Xie, Mingping ; Wang, Qi ; Wang, Lifu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4719-610a1c204bb46583ef9d07101d6e12a9262342a9f6de38b2ae8f50157ba0f52e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Actin</topic><topic>Actin Cytoskeleton - metabolism</topic><topic>Actin Cytoskeleton - pathology</topic><topic>Adenocarcinoma</topic><topic>Aged</topic><topic>Cancer therapies</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Carcinoma, Pancreatic Ductal - metabolism</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>cdc42 GTP-Binding Protein - analysis</topic><topic>cdc42 GTP-Binding Protein - metabolism</topic><topic>Cdc42 protein</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell morphology</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Chromosomal Proteins, Non-Histone - analysis</topic><topic>Chromosomal Proteins, Non-Histone - metabolism</topic><topic>Chromosomes</topic><topic>Cytochalasin B</topic><topic>Cytology</topic><topic>Cytoskeleton</topic><topic>Differentiation (biology)</topic><topic>Female</topic><topic>G2 Phase Cell Cycle Checkpoints</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Morphology</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Original</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Proteins</topic><topic>Quantitation</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Tong</creatorcontrib><creatorcontrib>Liu, Xu</creatorcontrib><creatorcontrib>Xu, Bin</creatorcontrib><creatorcontrib>Wu, Wei</creatorcontrib><creatorcontrib>Zang, Yi</creatorcontrib><creatorcontrib>Li, Juanjuan</creatorcontrib><creatorcontrib>Wei, Lumin</creatorcontrib><creatorcontrib>Qian, Yuting</creatorcontrib><creatorcontrib>Xu, Hui</creatorcontrib><creatorcontrib>Xie, Mingping</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Wang, Lifu</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell proliferation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Tong</au><au>Liu, Xu</au><au>Xu, Bin</au><au>Wu, Wei</au><au>Zang, Yi</au><au>Li, Juanjuan</au><au>Wei, Lumin</au><au>Qian, Yuting</au><au>Xu, Hui</au><au>Xie, Mingping</au><au>Wang, Qi</au><au>Wang, Lifu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SKA1 regulates actin cytoskeleton remodelling via activating Cdc42 and influences the migration of pancreatic ductal adenocarcinoma cells</atitle><jtitle>Cell proliferation</jtitle><addtitle>Cell Prolif</addtitle><date>2020-04</date><risdate>2020</risdate><volume>53</volume><issue>4</issue><spage>e12799</spage><epage>n/a</epage><pages>e12799-n/a</pages><issn>0960-7722</issn><eissn>1365-2184</eissn><abstract>Objectives
Spindle and kinetochore–associated protein 1(SKA1), originally identified as a protein essential for proper chromosome segregation, has been recently linked to multiple malignancies. This study aimed to explore the biological, clinical role and molecular mechanism of SKA1 in pancreatic carcinogenesis.
Materials and Methods
SKA1 expression was detected in 145 pancreatic ductal adenocarcinoma (PDAC) specimens by immunohistochemistry. Biological behaviour assays were used to determine the role of SKA1 in PDAC progression in vitro and in vivo. Using isobaric tags for relative and absolute quantitation (iTRAQ), SKA1’s downstream proteins were examined. Moreover, cytochalasin B and ZCL278 were used to explore the changes of SKA1‐induced signalling and cell morphology, with further confirmation by immunoblotting and immunofluorescence assays.
Results
Increased SKA1 expression was significantly correlated with tumour size and cellular differentiation degree in PDAC tissues. Furthermore, elevated levels of SKA1 reflected shorter overall survival (P = .019). As for biological behaviour, SKA1 acted as a tumour promotor in PDAC, overexpression of SKA1 facilitates cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, we demonstrated that SKA1 enhanced pancreatic cancer aggressiveness by inhibiting G2/M arrest and regulating actin cytoskeleton organization via activating Cdc42.
Conclusions
This study revealed novel roles for SKA1 as an important regulator of actin cytoskeleton organization and an oncogene in PDAC cells, which may provide insights into developing novel therapeutics.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32232899</pmid><doi>10.1111/cpr.12799</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-5172-9932</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Actin Actin Cytoskeleton - metabolism Actin Cytoskeleton - pathology Adenocarcinoma Aged Cancer therapies Carcinogenesis Carcinogens Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - pathology cdc42 GTP-Binding Protein - analysis cdc42 GTP-Binding Protein - metabolism Cdc42 protein Cell adhesion & migration Cell cycle Cell growth Cell Line, Tumor Cell migration Cell morphology Cell Movement Cell Proliferation Chromosomal Proteins, Non-Histone - analysis Chromosomal Proteins, Non-Histone - metabolism Chromosomes Cytochalasin B Cytology Cytoskeleton Differentiation (biology) Female G2 Phase Cell Cycle Checkpoints Gene expression Humans Immunoblotting Immunofluorescence Immunohistochemistry Male Metastasis Middle Aged Morphology Neoplasm Invasiveness - pathology Original Pancreatic cancer Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Proteins Quantitation Tumors |
| title | SKA1 regulates actin cytoskeleton remodelling via activating Cdc42 and influences the migration of pancreatic ductal adenocarcinoma cells |
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