PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial–mesenchymal transition
Background and Purpose PEP06, a polypeptide modified from endostatin, was investigated for its antitumour effects on colorectal cancer (CRC) and the possible mechanisms of this antitumour activity were examined in in vitro and in vivo models. Experimental Approach After PEP06 treatment, cell prolife...
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Veröffentlicht in: | British journal of pharmacology 2018-08, Vol.175 (15), p.3111-3130 |
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creator | Yu, Siming Li, Linna Tian, Wei Nie, Dan Mu, Wei Qiu, Fang Liu, Yu Liu, Xinghan Wang, Xiaofeng Du, Zhimin Chu, Wen‐Feng Yang, Baofeng |
description | Background and Purpose
PEP06, a polypeptide modified from endostatin, was investigated for its antitumour effects on colorectal cancer (CRC) and the possible mechanisms of this antitumour activity were examined in in vitro and in vivo models.
Experimental Approach
After PEP06 treatment, cell proliferation and migration assays were performed in CRC cells. Epithelial–mesenchymal transition (EMT) progression was determined by Western blotting, immunofluorescent staining and immunohistochemistry in vitro and in a residual xenograft model. MiRNAs regulated by PEP06 were identified by miRNA microarray and verified by in situ hybridization and quantitative real‐time PCR. The interactions between PEP06 and integrin αvβ3 were determined with Biacore SA biochips. The cellular function of miR‐146b‐5p was validated by gain‐of‐function and loss‐of‐function approaches. A mouse model of lung metastasis was used to determine the effect of PEP06 on metastatic growth.
Key Results
PEP06 did not affect cell viability but reduced migration and EMT in SW620 and HCT116 cells. PEP06 significantly repressed the expression of miR‐146b‐5p in these two cell lines through binding to integrin αvβ3. MiR‐146b‐5p was shown to increase EMT by targeting Smad4, and the miR‐146b‐5p‐Smad4 cascade regulated EMT in CRC. PEP06 also suppressed CRC pulmonary metastasis, increased survival of mice and hampered residual tumour growth by inhibiting EMT through down‐regulating miR‐146b‐5p.
Conclusions and Implications
PEP06 is a polypeptide that inhibits the growth and metastasis of colon cancer through its RGD motif binding to integrin αvβ3, thereby down‐regulating miR‐146b‐5p to inhibit EMT in vitro and in vivo. It might have potential as a therapeutic for CRC. |
doi_str_mv | 10.1111/bph.14352 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6031886</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2064075737</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4432-b72777963ff47670041becb6867ebf758c1767e5727060ef75d0bb37c80605cb3</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhi1URLctB14AWeqJQ1o7TuzsBalULUWqxB7o2bK9k8ZVYgfbW7o33oE35EkY2FLRA77Ynvnm93h-Qt5wdsJxndp5OOGNaOsXZMEbJatWdHyPLBhjquK86_bJQc53jGFSta_Ifr1Udb0UfEEeVhcrJukcx-0Mc_FroIJReIBUMjWh-LKZ4iZR6HtwhfpAXRxjwrMZqTPJ-RAnQ--9wdzgrS8-3FKYfRlg9Gb8-f3HBBmCG7YTVpRkQkYmhiPysjdjhteP-yG5ubz4cn5VXX_--On87LpyTSPqyqpaKbWUou_xY4qxhltwVnZSge1V2zmOYWgRY5IBRtbMWqFch9fWWXFI3u90542dYO0gYA-jnpOfTNrqaLx-ngl-0LfxXksmcHISBY4fBVL8uoFc9B0OJGDPumayYapVQiH1bke5FHNO0D-9wJn-bZJGk_Qfk5B9-29LT-RfVxA43QHf_Ajb_yvpD6urneQv7gKezQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2064075737</pqid></control><display><type>article</type><title>PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial–mesenchymal transition</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Yu, Siming ; Li, Linna ; Tian, Wei ; Nie, Dan ; Mu, Wei ; Qiu, Fang ; Liu, Yu ; Liu, Xinghan ; Wang, Xiaofeng ; Du, Zhimin ; Chu, Wen‐Feng ; Yang, Baofeng</creator><creatorcontrib>Yu, Siming ; Li, Linna ; Tian, Wei ; Nie, Dan ; Mu, Wei ; Qiu, Fang ; Liu, Yu ; Liu, Xinghan ; Wang, Xiaofeng ; Du, Zhimin ; Chu, Wen‐Feng ; Yang, Baofeng</creatorcontrib><description>Background and Purpose
PEP06, a polypeptide modified from endostatin, was investigated for its antitumour effects on colorectal cancer (CRC) and the possible mechanisms of this antitumour activity were examined in in vitro and in vivo models.
Experimental Approach
After PEP06 treatment, cell proliferation and migration assays were performed in CRC cells. Epithelial–mesenchymal transition (EMT) progression was determined by Western blotting, immunofluorescent staining and immunohistochemistry in vitro and in a residual xenograft model. MiRNAs regulated by PEP06 were identified by miRNA microarray and verified by in situ hybridization and quantitative real‐time PCR. The interactions between PEP06 and integrin αvβ3 were determined with Biacore SA biochips. The cellular function of miR‐146b‐5p was validated by gain‐of‐function and loss‐of‐function approaches. A mouse model of lung metastasis was used to determine the effect of PEP06 on metastatic growth.
Key Results
PEP06 did not affect cell viability but reduced migration and EMT in SW620 and HCT116 cells. PEP06 significantly repressed the expression of miR‐146b‐5p in these two cell lines through binding to integrin αvβ3. MiR‐146b‐5p was shown to increase EMT by targeting Smad4, and the miR‐146b‐5p‐Smad4 cascade regulated EMT in CRC. PEP06 also suppressed CRC pulmonary metastasis, increased survival of mice and hampered residual tumour growth by inhibiting EMT through down‐regulating miR‐146b‐5p.
Conclusions and Implications
PEP06 is a polypeptide that inhibits the growth and metastasis of colon cancer through its RGD motif binding to integrin αvβ3, thereby down‐regulating miR‐146b‐5p to inhibit EMT in vitro and in vivo. It might have potential as a therapeutic for CRC.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/bph.14352</identifier><identifier>PMID: 29722931</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animal models ; Animals ; Antigens, CD - metabolism ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Biochips ; Cadherins - metabolism ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell proliferation ; Colon cancer ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Endostatin ; Epithelial-Mesenchymal Transition - drug effects ; Female ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - physiology ; Humans ; Immunohistochemistry ; Lung Neoplasms - secondary ; Lungs ; Mesenchyme ; Metastases ; Metastasis ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - metabolism ; miRNA ; Polypeptides ; Research Paper ; Research Papers ; Smad4 protein ; Tumors ; Vimentin - metabolism ; Western blotting ; Wound Healing - drug effects ; Xenografts</subject><ispartof>British journal of pharmacology, 2018-08, Vol.175 (15), p.3111-3130</ispartof><rights>2018 The British Pharmacological Society</rights><rights>2018 The British Pharmacological Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4432-b72777963ff47670041becb6867ebf758c1767e5727060ef75d0bb37c80605cb3</citedby><cites>FETCH-LOGICAL-c4432-b72777963ff47670041becb6867ebf758c1767e5727060ef75d0bb37c80605cb3</cites><orcidid>0000-0002-0125-1608 ; 0000-0002-6672-3979</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/PMC6031886/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031886/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29722931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Siming</creatorcontrib><creatorcontrib>Li, Linna</creatorcontrib><creatorcontrib>Tian, Wei</creatorcontrib><creatorcontrib>Nie, Dan</creatorcontrib><creatorcontrib>Mu, Wei</creatorcontrib><creatorcontrib>Qiu, Fang</creatorcontrib><creatorcontrib>Liu, Yu</creatorcontrib><creatorcontrib>Liu, Xinghan</creatorcontrib><creatorcontrib>Wang, Xiaofeng</creatorcontrib><creatorcontrib>Du, Zhimin</creatorcontrib><creatorcontrib>Chu, Wen‐Feng</creatorcontrib><creatorcontrib>Yang, Baofeng</creatorcontrib><title>PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial–mesenchymal transition</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and Purpose
PEP06, a polypeptide modified from endostatin, was investigated for its antitumour effects on colorectal cancer (CRC) and the possible mechanisms of this antitumour activity were examined in in vitro and in vivo models.
Experimental Approach
After PEP06 treatment, cell proliferation and migration assays were performed in CRC cells. Epithelial–mesenchymal transition (EMT) progression was determined by Western blotting, immunofluorescent staining and immunohistochemistry in vitro and in a residual xenograft model. MiRNAs regulated by PEP06 were identified by miRNA microarray and verified by in situ hybridization and quantitative real‐time PCR. The interactions between PEP06 and integrin αvβ3 were determined with Biacore SA biochips. The cellular function of miR‐146b‐5p was validated by gain‐of‐function and loss‐of‐function approaches. A mouse model of lung metastasis was used to determine the effect of PEP06 on metastatic growth.
Key Results
PEP06 did not affect cell viability but reduced migration and EMT in SW620 and HCT116 cells. PEP06 significantly repressed the expression of miR‐146b‐5p in these two cell lines through binding to integrin αvβ3. MiR‐146b‐5p was shown to increase EMT by targeting Smad4, and the miR‐146b‐5p‐Smad4 cascade regulated EMT in CRC. PEP06 also suppressed CRC pulmonary metastasis, increased survival of mice and hampered residual tumour growth by inhibiting EMT through down‐regulating miR‐146b‐5p.
Conclusions and Implications
PEP06 is a polypeptide that inhibits the growth and metastasis of colon cancer through its RGD motif binding to integrin αvβ3, thereby down‐regulating miR‐146b‐5p to inhibit EMT in vitro and in vivo. It might have potential as a therapeutic for CRC.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antigens, CD - metabolism</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Biochips</subject><subject>Cadherins - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Endostatin</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Female</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - physiology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lung Neoplasms - secondary</subject><subject>Lungs</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Polypeptides</subject><subject>Research Paper</subject><subject>Research Papers</subject><subject>Smad4 protein</subject><subject>Tumors</subject><subject>Vimentin - metabolism</subject><subject>Western blotting</subject><subject>Wound Healing - drug effects</subject><subject>Xenografts</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFu1DAQhi1URLctB14AWeqJQ1o7TuzsBalULUWqxB7o2bK9k8ZVYgfbW7o33oE35EkY2FLRA77Ynvnm93h-Qt5wdsJxndp5OOGNaOsXZMEbJatWdHyPLBhjquK86_bJQc53jGFSta_Ifr1Udb0UfEEeVhcrJukcx-0Mc_FroIJReIBUMjWh-LKZ4iZR6HtwhfpAXRxjwrMZqTPJ-RAnQ--9wdzgrS8-3FKYfRlg9Gb8-f3HBBmCG7YTVpRkQkYmhiPysjdjhteP-yG5ubz4cn5VXX_--On87LpyTSPqyqpaKbWUou_xY4qxhltwVnZSge1V2zmOYWgRY5IBRtbMWqFch9fWWXFI3u90542dYO0gYA-jnpOfTNrqaLx-ngl-0LfxXksmcHISBY4fBVL8uoFc9B0OJGDPumayYapVQiH1bke5FHNO0D-9wJn-bZJGk_Qfk5B9-29LT-RfVxA43QHf_Ajb_yvpD6urneQv7gKezQ</recordid><startdate>201808</startdate><enddate>201808</enddate><creator>Yu, Siming</creator><creator>Li, Linna</creator><creator>Tian, Wei</creator><creator>Nie, Dan</creator><creator>Mu, Wei</creator><creator>Qiu, Fang</creator><creator>Liu, Yu</creator><creator>Liu, Xinghan</creator><creator>Wang, Xiaofeng</creator><creator>Du, Zhimin</creator><creator>Chu, Wen‐Feng</creator><creator>Yang, Baofeng</creator><general>Blackwell Publishing Ltd</general><general>John Wiley and Sons Inc</general><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>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0125-1608</orcidid><orcidid>https://orcid.org/0000-0002-6672-3979</orcidid></search><sort><creationdate>201808</creationdate><title>PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial–mesenchymal transition</title><author>Yu, Siming ; Li, Linna ; Tian, Wei ; Nie, Dan ; Mu, Wei ; Qiu, Fang ; Liu, Yu ; Liu, Xinghan ; Wang, Xiaofeng ; Du, Zhimin ; Chu, Wen‐Feng ; Yang, Baofeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4432-b72777963ff47670041becb6867ebf758c1767e5727060ef75d0bb37c80605cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antigens, CD - metabolism</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Biochips</topic><topic>Cadherins - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Endostatin</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Female</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Human Umbilical Vein Endothelial Cells - physiology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Lung Neoplasms - secondary</topic><topic>Lungs</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Polypeptides</topic><topic>Research Paper</topic><topic>Research Papers</topic><topic>Smad4 protein</topic><topic>Tumors</topic><topic>Vimentin - metabolism</topic><topic>Western blotting</topic><topic>Wound Healing - drug effects</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Siming</creatorcontrib><creatorcontrib>Li, Linna</creatorcontrib><creatorcontrib>Tian, Wei</creatorcontrib><creatorcontrib>Nie, Dan</creatorcontrib><creatorcontrib>Mu, Wei</creatorcontrib><creatorcontrib>Qiu, Fang</creatorcontrib><creatorcontrib>Liu, Yu</creatorcontrib><creatorcontrib>Liu, Xinghan</creatorcontrib><creatorcontrib>Wang, Xiaofeng</creatorcontrib><creatorcontrib>Du, Zhimin</creatorcontrib><creatorcontrib>Chu, Wen‐Feng</creatorcontrib><creatorcontrib>Yang, Baofeng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Siming</au><au>Li, Linna</au><au>Tian, Wei</au><au>Nie, Dan</au><au>Mu, Wei</au><au>Qiu, Fang</au><au>Liu, Yu</au><au>Liu, Xinghan</au><au>Wang, Xiaofeng</au><au>Du, Zhimin</au><au>Chu, Wen‐Feng</au><au>Yang, Baofeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial–mesenchymal transition</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2018-08</date><risdate>2018</risdate><volume>175</volume><issue>15</issue><spage>3111</spage><epage>3130</epage><pages>3111-3130</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>Background and Purpose
PEP06, a polypeptide modified from endostatin, was investigated for its antitumour effects on colorectal cancer (CRC) and the possible mechanisms of this antitumour activity were examined in in vitro and in vivo models.
Experimental Approach
After PEP06 treatment, cell proliferation and migration assays were performed in CRC cells. Epithelial–mesenchymal transition (EMT) progression was determined by Western blotting, immunofluorescent staining and immunohistochemistry in vitro and in a residual xenograft model. MiRNAs regulated by PEP06 were identified by miRNA microarray and verified by in situ hybridization and quantitative real‐time PCR. The interactions between PEP06 and integrin αvβ3 were determined with Biacore SA biochips. The cellular function of miR‐146b‐5p was validated by gain‐of‐function and loss‐of‐function approaches. A mouse model of lung metastasis was used to determine the effect of PEP06 on metastatic growth.
Key Results
PEP06 did not affect cell viability but reduced migration and EMT in SW620 and HCT116 cells. PEP06 significantly repressed the expression of miR‐146b‐5p in these two cell lines through binding to integrin αvβ3. MiR‐146b‐5p was shown to increase EMT by targeting Smad4, and the miR‐146b‐5p‐Smad4 cascade regulated EMT in CRC. PEP06 also suppressed CRC pulmonary metastasis, increased survival of mice and hampered residual tumour growth by inhibiting EMT through down‐regulating miR‐146b‐5p.
Conclusions and Implications
PEP06 is a polypeptide that inhibits the growth and metastasis of colon cancer through its RGD motif binding to integrin αvβ3, thereby down‐regulating miR‐146b‐5p to inhibit EMT in vitro and in vivo. It might have potential as a therapeutic for CRC.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>29722931</pmid><doi>10.1111/bph.14352</doi><tpages>20</tpages><orcidid>https://orcid.org/0000-0002-0125-1608</orcidid><orcidid>https://orcid.org/0000-0002-6672-3979</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animal models Animals Antigens, CD - metabolism Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Biochips Cadherins - metabolism Cell Line, Tumor Cell migration Cell Movement - drug effects Cell proliferation Colon cancer Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Endostatin Epithelial-Mesenchymal Transition - drug effects Female Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - physiology Humans Immunohistochemistry Lung Neoplasms - secondary Lungs Mesenchyme Metastases Metastasis Mice, Inbred BALB C Mice, Nude MicroRNAs - metabolism miRNA Polypeptides Research Paper Research Papers Smad4 protein Tumors Vimentin - metabolism Western blotting Wound Healing - drug effects Xenografts |
title | PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial–mesenchymal transition |
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