C‑C chemokine receptor type 2 promotes epithelial‑to‑mesenchymal transition by upregulating matrix metalloproteinase‑2 in human liver cancer
C‑C chemokine receptor type 2 (CCR2) is aberrantly expressed in a variety of tumor cells, and participates in the regulation of tumor cell progression, metastasis and immune escape. However, the mechanism of action of CCR2 in liver cancer remains unclear. In the present study, the aim was to elucida...
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| Veröffentlicht in: | Oncology reports 2018-11, Vol.40 (5), p.2734-2741 |
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| creator | Li, Huijin Li, Hui Li, Xiao-Peng Zou, Haojun Liu, Liting Liu, Wangqiao Duan, Tao |
| description | C‑C chemokine receptor type 2 (CCR2) is aberrantly expressed in a variety of tumor cells, and participates in the regulation of tumor cell progression, metastasis and immune escape. However, the mechanism of action of CCR2 in liver cancer remains unclear. In the present study, the aim was to elucidate the molecular mechanism underlying the regulation of epithelial‑to‑mesenchymal transition (EMT) by CCR2 in liver cancer cells. Initially, CCR2 expression in liver cancer tissues was measured, and the survival time of patients was analyzed by Kaplan‑Meier analysis. In liver cancer cells, the mRNA and protein expression levels of CCR2, matrix metalloproteinase‑2 (MMP2), E‑cadherin and vimentin were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blotting. Cell viability, migration and invasion were determined by Cell Counting Kit‑8, wound healing and Transwell chamber assays, respectively. Additionally, the binding between CCR2 and MMP2 was identified by co‑immunoprecipitation (Co‑IP). It was observed that CCR2 was abnormally upregulated in liver cancer tissues and significantly associated with the tumor diameter, metastasis and stage. The survival of patients with high CCR2 expression was lower compared with that of patients with low CCR2 expression. In addition, the number of cells that penetrated the transwell chamber membrane was significantly reduced following treatment with CCR2‑small interfering RNA (siRNA). Furthermore, CCR2 was found to participate in MMP2‑induced EMT, while CCR2‑siRNA transfection reduced the expression and activity of MMP2, and confirmed the specific binding between CCR2 and MMP2. Co‑IP also identified the independent interaction between endogenous proteins in HepG2 cells. These results revealed that CCR2 promotes EMT in liver cancer. Thus, CCR2 is an attractive novel target for inhibiting invasion and metastasis of liver cancer cells. |
| doi_str_mv | 10.3892/or.2018.6660 |
| format | Article |
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However, the mechanism of action of CCR2 in liver cancer remains unclear. In the present study, the aim was to elucidate the molecular mechanism underlying the regulation of epithelial‑to‑mesenchymal transition (EMT) by CCR2 in liver cancer cells. Initially, CCR2 expression in liver cancer tissues was measured, and the survival time of patients was analyzed by Kaplan‑Meier analysis. In liver cancer cells, the mRNA and protein expression levels of CCR2, matrix metalloproteinase‑2 (MMP2), E‑cadherin and vimentin were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blotting. Cell viability, migration and invasion were determined by Cell Counting Kit‑8, wound healing and Transwell chamber assays, respectively. Additionally, the binding between CCR2 and MMP2 was identified by co‑immunoprecipitation (Co‑IP). It was observed that CCR2 was abnormally upregulated in liver cancer tissues and significantly associated with the tumor diameter, metastasis and stage. The survival of patients with high CCR2 expression was lower compared with that of patients with low CCR2 expression. In addition, the number of cells that penetrated the transwell chamber membrane was significantly reduced following treatment with CCR2‑small interfering RNA (siRNA). Furthermore, CCR2 was found to participate in MMP2‑induced EMT, while CCR2‑siRNA transfection reduced the expression and activity of MMP2, and confirmed the specific binding between CCR2 and MMP2. Co‑IP also identified the independent interaction between endogenous proteins in HepG2 cells. These results revealed that CCR2 promotes EMT in liver cancer. Thus, CCR2 is an attractive novel target for inhibiting invasion and metastasis of liver cancer cells.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2018.6660</identifier><identifier>PMID: 30132565</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Care and treatment ; Cell receptors ; Chemokines ; Development and progression ; Gene expression ; Genetic aspects ; Health aspects ; Immunoglobulins ; Liver cancer ; Metastasis ; Polymerase chain reaction ; Proteins ; Survival analysis</subject><ispartof>Oncology reports, 2018-11, Vol.40 (5), p.2734-2741</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-cd5ba0e5d6885d4c6f8f979c45d024bfaef7df96af66d5f4bc98cc20325461cd3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30132565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Huijin</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Li, Xiao-Peng</creatorcontrib><creatorcontrib>Zou, Haojun</creatorcontrib><creatorcontrib>Liu, Liting</creatorcontrib><creatorcontrib>Liu, Wangqiao</creatorcontrib><creatorcontrib>Duan, Tao</creatorcontrib><title>C‑C chemokine receptor type 2 promotes epithelial‑to‑mesenchymal transition by upregulating matrix metalloproteinase‑2 in human liver cancer</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>C‑C chemokine receptor type 2 (CCR2) is aberrantly expressed in a variety of tumor cells, and participates in the regulation of tumor cell progression, metastasis and immune escape. However, the mechanism of action of CCR2 in liver cancer remains unclear. In the present study, the aim was to elucidate the molecular mechanism underlying the regulation of epithelial‑to‑mesenchymal transition (EMT) by CCR2 in liver cancer cells. Initially, CCR2 expression in liver cancer tissues was measured, and the survival time of patients was analyzed by Kaplan‑Meier analysis. In liver cancer cells, the mRNA and protein expression levels of CCR2, matrix metalloproteinase‑2 (MMP2), E‑cadherin and vimentin were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blotting. Cell viability, migration and invasion were determined by Cell Counting Kit‑8, wound healing and Transwell chamber assays, respectively. Additionally, the binding between CCR2 and MMP2 was identified by co‑immunoprecipitation (Co‑IP). It was observed that CCR2 was abnormally upregulated in liver cancer tissues and significantly associated with the tumor diameter, metastasis and stage. The survival of patients with high CCR2 expression was lower compared with that of patients with low CCR2 expression. In addition, the number of cells that penetrated the transwell chamber membrane was significantly reduced following treatment with CCR2‑small interfering RNA (siRNA). Furthermore, CCR2 was found to participate in MMP2‑induced EMT, while CCR2‑siRNA transfection reduced the expression and activity of MMP2, and confirmed the specific binding between CCR2 and MMP2. Co‑IP also identified the independent interaction between endogenous proteins in HepG2 cells. These results revealed that CCR2 promotes EMT in liver cancer. Thus, CCR2 is an attractive novel target for inhibiting invasion and metastasis of liver cancer cells.</description><subject>Care and treatment</subject><subject>Cell receptors</subject><subject>Chemokines</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Immunoglobulins</subject><subject>Liver cancer</subject><subject>Metastasis</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Survival analysis</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptksuKFDEUhgtRnHF051oCgriw2iRVSVUth2a8wIAbBXchnTrpyphLmaTE3vkKs3Dvs_goPokpZryMSCAJyff_nHP4q-ohwZumH-jzEDcUk37DOce3qmPSDaSmbUNulzumpG4a9v6oupfSBca0w3y4Wx01mDSUcXZcfd3--HK5RWoCFz4YDyiCgjmHiPJhhu_fKJpjcCFDQjCbPIE10hZJDmVzkMCr6eCkRTlKn0w2waPdAS1zhP1iZTZ-j5zM0XxGDrK0NhS_DMbLBMWBIuPRtDjpkTWfICIlvYJ4v7qjpU3w4Po8qd69OHu7fVWfv3n5ent6XquWsVyrke0kBjbyvmdjq7ju9dAN5XPEtN1pCbob9cCl5nxkut2poVeK4tJ7y4kam5Pq6ZVvKerjAikLZ5ICa6WHsCRB8UB6wpquK-jjf9CLsERfqhOUEIIHRjvyh9pLC8J4Hcpc1GoqThnrWo4bvHpt_kOVNYIzKnjQprzfEDz5SzCBtHlKwS7ruNNN8NkVqGJIKYIWczROxoMgWKxxESGKNS5ijUvBH103tewcjL_hX_lofgLE8MDc</recordid><startdate>20181101</startdate><enddate>20181101</enddate><creator>Li, Huijin</creator><creator>Li, Hui</creator><creator>Li, Xiao-Peng</creator><creator>Zou, Haojun</creator><creator>Liu, Liting</creator><creator>Liu, Wangqiao</creator><creator>Duan, Tao</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20181101</creationdate><title>C‑C chemokine receptor type 2 promotes epithelial‑to‑mesenchymal transition by upregulating matrix metalloproteinase‑2 in human liver cancer</title><author>Li, Huijin ; Li, Hui ; Li, Xiao-Peng ; Zou, Haojun ; Liu, Liting ; Liu, Wangqiao ; Duan, Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-cd5ba0e5d6885d4c6f8f979c45d024bfaef7df96af66d5f4bc98cc20325461cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Care and treatment</topic><topic>Cell receptors</topic><topic>Chemokines</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Immunoglobulins</topic><topic>Liver cancer</topic><topic>Metastasis</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Survival analysis</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Huijin</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Li, Xiao-Peng</creatorcontrib><creatorcontrib>Zou, Haojun</creatorcontrib><creatorcontrib>Liu, Liting</creatorcontrib><creatorcontrib>Liu, Wangqiao</creatorcontrib><creatorcontrib>Duan, Tao</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Huijin</au><au>Li, Hui</au><au>Li, Xiao-Peng</au><au>Zou, Haojun</au><au>Liu, Liting</au><au>Liu, Wangqiao</au><au>Duan, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C‑C chemokine receptor type 2 promotes epithelial‑to‑mesenchymal transition by upregulating matrix metalloproteinase‑2 in human liver cancer</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2018-11-01</date><risdate>2018</risdate><volume>40</volume><issue>5</issue><spage>2734</spage><epage>2741</epage><pages>2734-2741</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>C‑C chemokine receptor type 2 (CCR2) is aberrantly expressed in a variety of tumor cells, and participates in the regulation of tumor cell progression, metastasis and immune escape. However, the mechanism of action of CCR2 in liver cancer remains unclear. In the present study, the aim was to elucidate the molecular mechanism underlying the regulation of epithelial‑to‑mesenchymal transition (EMT) by CCR2 in liver cancer cells. Initially, CCR2 expression in liver cancer tissues was measured, and the survival time of patients was analyzed by Kaplan‑Meier analysis. In liver cancer cells, the mRNA and protein expression levels of CCR2, matrix metalloproteinase‑2 (MMP2), E‑cadherin and vimentin were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blotting. Cell viability, migration and invasion were determined by Cell Counting Kit‑8, wound healing and Transwell chamber assays, respectively. Additionally, the binding between CCR2 and MMP2 was identified by co‑immunoprecipitation (Co‑IP). It was observed that CCR2 was abnormally upregulated in liver cancer tissues and significantly associated with the tumor diameter, metastasis and stage. The survival of patients with high CCR2 expression was lower compared with that of patients with low CCR2 expression. In addition, the number of cells that penetrated the transwell chamber membrane was significantly reduced following treatment with CCR2‑small interfering RNA (siRNA). Furthermore, CCR2 was found to participate in MMP2‑induced EMT, while CCR2‑siRNA transfection reduced the expression and activity of MMP2, and confirmed the specific binding between CCR2 and MMP2. Co‑IP also identified the independent interaction between endogenous proteins in HepG2 cells. These results revealed that CCR2 promotes EMT in liver cancer. Thus, CCR2 is an attractive novel target for inhibiting invasion and metastasis of liver cancer cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30132565</pmid><doi>10.3892/or.2018.6660</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology reports, 2018-11, Vol.40 (5), p.2734-2741 |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Care and treatment Cell receptors Chemokines Development and progression Gene expression Genetic aspects Health aspects Immunoglobulins Liver cancer Metastasis Polymerase chain reaction Proteins Survival analysis |
| title | C‑C chemokine receptor type 2 promotes epithelial‑to‑mesenchymal transition by upregulating matrix metalloproteinase‑2 in human liver cancer |
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