CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells
C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrate...
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| Veröffentlicht in: | Oncology letters 2017-12, Vol.14 (6), p.7977-7985 |
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| creator | Yang, Yang Hou, Jie Shao, Mingliang Zhang, Wei Qi, Yaling E, Shengnan Wang, Shuqiu Sui, Hongyu Meng, Dexin Wang, Baixin Wang, Mingfu Han, Yang Cao, Yu Huang, Xiaoqing Li, Yue Zhang, Pengxia Wang, Weiqun |
| description | C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma. |
| doi_str_mv | 10.3892/ol.2017.7236 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5755189</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A526575261</galeid><sourcerecordid>A526575261</sourcerecordid><originalsourceid>FETCH-LOGICAL-c539t-c58692ff2dfc3adf9bc18673e5dda6472194d1942e274fa2730ffb1579ad68763</originalsourceid><addsrcrecordid>eNptkttrFDEUhwdRbKl981kCivjgrpPM5PZSKEtthYW-KPgWsrnspGYmY5JR-983465rV8wh9y-_k5ycqnoJ62XDOPoQ_BLVkC4pasiT6hRSjhawZujpYUzbk-o8pbu6FEwgY-R5dYJ407aorU-rX6uvqzUGMgE5ADnloKIbDAgRjDLK3UTd5_BtHrhCpRSUk9lo8NPlDowxeGdNlNmFIjBo0LvtfhYs6Mwoc9h4mXLoJbgx4zUCynifXlTPrPTJnO_7s-rLx6vPq5vF-vb60-pyvVC44bm0jHBkLdJWNVJbvlGQEdoYrLUkLUWQt7pUZBBtrUS0qa3dQEy51IRR0pxVFzvdcdr0Risz5Ci9GKPrZbwXQTpxvDO4TmzDD4EpxpDxIvBuLxDD98mkLHqX5ifIwYQpCcgZL5ckeEZf_4PehSkO5XkzxShlrMV_qa30RrjBhuJXzaLiEiNS_CICC7X8D1VMm96pMBjryvrRgbePDnRG-tyl4Kf5K9Ix-H4HqhhSisYeggFrMWeVCF7MWSXmrCr4q8cBPMB_cqgAb3ZAGsv_Ox3SgbldL-piv3UeANbf0tI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1988778845</pqid></control><display><type>article</type><title>CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells</title><source>Spandidos Publications Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Yang, Yang ; Hou, Jie ; Shao, Mingliang ; Zhang, Wei ; Qi, Yaling ; E, Shengnan ; Wang, Shuqiu ; Sui, Hongyu ; Meng, Dexin ; Wang, Baixin ; Wang, Mingfu ; Han, Yang ; Cao, Yu ; Huang, Xiaoqing ; Li, Yue ; Zhang, Pengxia ; Wang, Weiqun</creator><creatorcontrib>Yang, Yang ; Hou, Jie ; Shao, Mingliang ; Zhang, Wei ; Qi, Yaling ; E, Shengnan ; Wang, Shuqiu ; Sui, Hongyu ; Meng, Dexin ; Wang, Baixin ; Wang, Mingfu ; Han, Yang ; Cao, Yu ; Huang, Xiaoqing ; Li, Yue ; Zhang, Pengxia ; Wang, Weiqun</creatorcontrib><description>C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2017.7236</identifier><identifier>PMID: 29344240</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Angiogenesis ; autocrine ; Biotechnology industry ; C-X-C motif chemokine ligand 5 ; Care and treatment ; Cell growth ; Cell receptors ; Chemokines ; Cytokines ; Development and progression ; Gene expression ; Genes ; Genetic aspects ; Health aspects ; hepatoblastoma ; Hypotheses ; Ligands ; Liver cancer ; Lymphoma ; Metastasis ; Oncology ; paracrine ; Polyclonal antibodies ; Polymerase chain reaction ; Proteins ; Rodents ; Studies ; Tumors ; Vascular endothelial growth factor</subject><ispartof>Oncology letters, 2017-12, Vol.14 (6), p.7977-7985</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright © 2017, Spandidos Publications 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-c58692ff2dfc3adf9bc18673e5dda6472194d1942e274fa2730ffb1579ad68763</citedby><cites>FETCH-LOGICAL-c539t-c58692ff2dfc3adf9bc18673e5dda6472194d1942e274fa2730ffb1579ad68763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755189/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755189/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,5556,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29344240$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Hou, Jie</creatorcontrib><creatorcontrib>Shao, Mingliang</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Qi, Yaling</creatorcontrib><creatorcontrib>E, Shengnan</creatorcontrib><creatorcontrib>Wang, Shuqiu</creatorcontrib><creatorcontrib>Sui, Hongyu</creatorcontrib><creatorcontrib>Meng, Dexin</creatorcontrib><creatorcontrib>Wang, Baixin</creatorcontrib><creatorcontrib>Wang, Mingfu</creatorcontrib><creatorcontrib>Han, Yang</creatorcontrib><creatorcontrib>Cao, Yu</creatorcontrib><creatorcontrib>Huang, Xiaoqing</creatorcontrib><creatorcontrib>Li, Yue</creatorcontrib><creatorcontrib>Zhang, Pengxia</creatorcontrib><creatorcontrib>Wang, Weiqun</creatorcontrib><title>CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma.</description><subject>Angiogenesis</subject><subject>autocrine</subject><subject>Biotechnology industry</subject><subject>C-X-C motif chemokine ligand 5</subject><subject>Care and treatment</subject><subject>Cell growth</subject><subject>Cell receptors</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>hepatoblastoma</subject><subject>Hypotheses</subject><subject>Ligands</subject><subject>Liver cancer</subject><subject>Lymphoma</subject><subject>Metastasis</subject><subject>Oncology</subject><subject>paracrine</subject><subject>Polyclonal antibodies</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Studies</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkttrFDEUhwdRbKl981kCivjgrpPM5PZSKEtthYW-KPgWsrnspGYmY5JR-983465rV8wh9y-_k5ycqnoJ62XDOPoQ_BLVkC4pasiT6hRSjhawZujpYUzbk-o8pbu6FEwgY-R5dYJ407aorU-rX6uvqzUGMgE5ADnloKIbDAgRjDLK3UTd5_BtHrhCpRSUk9lo8NPlDowxeGdNlNmFIjBo0LvtfhYs6Mwoc9h4mXLoJbgx4zUCynifXlTPrPTJnO_7s-rLx6vPq5vF-vb60-pyvVC44bm0jHBkLdJWNVJbvlGQEdoYrLUkLUWQt7pUZBBtrUS0qa3dQEy51IRR0pxVFzvdcdr0Risz5Ci9GKPrZbwXQTpxvDO4TmzDD4EpxpDxIvBuLxDD98mkLHqX5ifIwYQpCcgZL5ckeEZf_4PehSkO5XkzxShlrMV_qa30RrjBhuJXzaLiEiNS_CICC7X8D1VMm96pMBjryvrRgbePDnRG-tyl4Kf5K9Ix-H4HqhhSisYeggFrMWeVCF7MWSXmrCr4q8cBPMB_cqgAb3ZAGsv_Ox3SgbldL-piv3UeANbf0tI</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Yang, Yang</creator><creator>Hou, Jie</creator><creator>Shao, Mingliang</creator><creator>Zhang, Wei</creator><creator>Qi, Yaling</creator><creator>E, Shengnan</creator><creator>Wang, Shuqiu</creator><creator>Sui, Hongyu</creator><creator>Meng, Dexin</creator><creator>Wang, Baixin</creator><creator>Wang, Mingfu</creator><creator>Han, Yang</creator><creator>Cao, Yu</creator><creator>Huang, Xiaoqing</creator><creator>Li, Yue</creator><creator>Zhang, Pengxia</creator><creator>Wang, Weiqun</creator><general>D.A. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Yang</au><au>Hou, Jie</au><au>Shao, Mingliang</au><au>Zhang, Wei</au><au>Qi, Yaling</au><au>E, Shengnan</au><au>Wang, Shuqiu</au><au>Sui, Hongyu</au><au>Meng, Dexin</au><au>Wang, Baixin</au><au>Wang, Mingfu</au><au>Han, Yang</au><au>Cao, Yu</au><au>Huang, Xiaoqing</au><au>Li, Yue</au><au>Zhang, Pengxia</au><au>Wang, Weiqun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>14</volume><issue>6</issue><spage>7977</spage><epage>7985</epage><pages>7977-7985</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>29344240</pmid><doi>10.3892/ol.2017.7236</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology letters, 2017-12, Vol.14 (6), p.7977-7985 |
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| source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Angiogenesis autocrine Biotechnology industry C-X-C motif chemokine ligand 5 Care and treatment Cell growth Cell receptors Chemokines Cytokines Development and progression Gene expression Genes Genetic aspects Health aspects hepatoblastoma Hypotheses Ligands Liver cancer Lymphoma Metastasis Oncology paracrine Polyclonal antibodies Polymerase chain reaction Proteins Rodents Studies Tumors Vascular endothelial growth factor |
| title | CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells |
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