C‐C chemokine hepatocellular carcinoma motif ligand 5‐deficiency promotes hepatocellular carcinoma progression by affecting B cell recruitment

Objective To evaluate the expression of C‐C motif chemokine ligand 5 (CCL5) in hepatocellular carcinoma (HCC) and to explore its role in regulating the immune microenvironment and the related mechanism in tumor immunity. Methods The mRNA expression level of CCL5 in HCC and adjacent non‐cancerous tis...

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Veröffentlicht in:Journal of digestive diseases 2021-07, Vol.22 (7), p.433-441
Hauptverfasser: Li, Xiang, Han, Qiu Cheng, Yu, Chang, Luo, Yi Chun, Wang, Fang, Sun, Xue Hua, Gao, Yue Qiu, Tan, Wei Feng, Xia, Qiang
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container_end_page 441
container_issue 7
container_start_page 433
container_title Journal of digestive diseases
container_volume 22
creator Li, Xiang
Han, Qiu Cheng
Yu, Chang
Luo, Yi Chun
Wang, Fang
Sun, Xue Hua
Gao, Yue Qiu
Tan, Wei Feng
Xia, Qiang
description Objective To evaluate the expression of C‐C motif chemokine ligand 5 (CCL5) in hepatocellular carcinoma (HCC) and to explore its role in regulating the immune microenvironment and the related mechanism in tumor immunity. Methods The mRNA expression level of CCL5 in HCC and adjacent non‐cancerous tissues was measured by quantitative polymerase chain reaction and the protein expression was examined by immunohistochemistry. Serum CCL5 expression was measured by an enzyme‐linked immunosorbent assay (ELISA). C57BL/6 wild‐type (WT) and Ccl5‐knockout (Ccl5−/−) mice were utilized to conduct the diethylnitrosamine‐induced HCC model. The immune cell population was determined by flow cytometry, and peripheral serum immunoglobulin M (IgM) level was quantified by ELISA. Results CCL5 expression was low in HCC tissue and peripheral blood compared with adjacent non‐cancerous tissues or controls, and its expression was correlated with the overall survival, cancer recurrence and distant metastasis. In the HCC mouse model, liver‐to‐body weight ratio was of the Ccl5−/− group were higher than that of the WT group. Moreover, compared with the WT mice, the number of B cells in the tumor tissue of the Ccl5−/− mice was lower, while there were no significant differences in the other immune cell populations. Furthermore, serum IgM level of the Ccl5−/− mice was significantly lower than that of the WT mice. Conclusion CCL5 expression is decreased in HCC tissues. CCL5 deficiency reduces B cell recruitment and decreases IgM secretion in HCC, potentially leading to tumor progression. CCL5 expression was low in hepatocellular carcinoma (HCC) tissue and peripheral blood of the HCC patients, and its expression was correlated with the overall survival, recurrence and metastasis of the tumor. Deficiency of CCL5 in hepatocellular carcinoma accelerates tumor progression by decreasing B‐cell recruitment and IgM secretion.
doi_str_mv 10.1111/1751-2980.12997
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Methods The mRNA expression level of CCL5 in HCC and adjacent non‐cancerous tissues was measured by quantitative polymerase chain reaction and the protein expression was examined by immunohistochemistry. Serum CCL5 expression was measured by an enzyme‐linked immunosorbent assay (ELISA). C57BL/6 wild‐type (WT) and Ccl5‐knockout (Ccl5−/−) mice were utilized to conduct the diethylnitrosamine‐induced HCC model. The immune cell population was determined by flow cytometry, and peripheral serum immunoglobulin M (IgM) level was quantified by ELISA. Results CCL5 expression was low in HCC tissue and peripheral blood compared with adjacent non‐cancerous tissues or controls, and its expression was correlated with the overall survival, cancer recurrence and distant metastasis. In the HCC mouse model, liver‐to‐body weight ratio was of the Ccl5−/− group were higher than that of the WT group. Moreover, compared with the WT mice, the number of B cells in the tumor tissue of the Ccl5−/− mice was lower, while there were no significant differences in the other immune cell populations. Furthermore, serum IgM level of the Ccl5−/− mice was significantly lower than that of the WT mice. Conclusion CCL5 expression is decreased in HCC tissues. CCL5 deficiency reduces B cell recruitment and decreases IgM secretion in HCC, potentially leading to tumor progression. CCL5 expression was low in hepatocellular carcinoma (HCC) tissue and peripheral blood of the HCC patients, and its expression was correlated with the overall survival, recurrence and metastasis of the tumor. Deficiency of CCL5 in hepatocellular carcinoma accelerates tumor progression by decreasing B‐cell recruitment and IgM secretion.</description><identifier>ISSN: 1751-2972</identifier><identifier>EISSN: 1751-2980</identifier><identifier>DOI: 10.1111/1751-2980.12997</identifier><language>eng</language><publisher>Melbourne: Wiley Publishing Asia Pty Ltd</publisher><subject>B cell recruitment ; Body weight ; chemokine CCL5 ; Chemokines ; Diethylnitrosamine ; disease progression ; Enzyme-linked immunosorbent assay ; Flow cytometry ; Gene expression ; Hepatocellular carcinoma ; hepatocellular carcinomaimmunoglobulin M ; Immunoglobulin M ; Immunohistochemistry ; Ligands ; Liver cancer ; Lymphocytes B ; Metastases ; Microenvironments ; Peripheral blood ; Polymerase chain reaction</subject><ispartof>Journal of digestive diseases, 2021-07, Vol.22 (7), p.433-441</ispartof><rights>2021 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley &amp; Sons Australia, Ltd.</rights><rights>2021 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley &amp; Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3487-2fea6edce7f3866bc8df1adebe5d765a07a34546d137d81d03a2577f8c2afebd3</citedby><cites>FETCH-LOGICAL-c3487-2fea6edce7f3866bc8df1adebe5d765a07a34546d137d81d03a2577f8c2afebd3</cites><orcidid>0000-0001-7644-1994</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1751-2980.12997$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1751-2980.12997$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids></links><search><creatorcontrib>Li, Xiang</creatorcontrib><creatorcontrib>Han, Qiu Cheng</creatorcontrib><creatorcontrib>Yu, Chang</creatorcontrib><creatorcontrib>Luo, Yi Chun</creatorcontrib><creatorcontrib>Wang, Fang</creatorcontrib><creatorcontrib>Sun, Xue Hua</creatorcontrib><creatorcontrib>Gao, Yue Qiu</creatorcontrib><creatorcontrib>Tan, Wei Feng</creatorcontrib><creatorcontrib>Xia, Qiang</creatorcontrib><title>C‐C chemokine hepatocellular carcinoma motif ligand 5‐deficiency promotes hepatocellular carcinoma progression by affecting B cell recruitment</title><title>Journal of digestive diseases</title><description>Objective To evaluate the expression of C‐C motif chemokine ligand 5 (CCL5) in hepatocellular carcinoma (HCC) and to explore its role in regulating the immune microenvironment and the related mechanism in tumor immunity. Methods The mRNA expression level of CCL5 in HCC and adjacent non‐cancerous tissues was measured by quantitative polymerase chain reaction and the protein expression was examined by immunohistochemistry. Serum CCL5 expression was measured by an enzyme‐linked immunosorbent assay (ELISA). C57BL/6 wild‐type (WT) and Ccl5‐knockout (Ccl5−/−) mice were utilized to conduct the diethylnitrosamine‐induced HCC model. The immune cell population was determined by flow cytometry, and peripheral serum immunoglobulin M (IgM) level was quantified by ELISA. Results CCL5 expression was low in HCC tissue and peripheral blood compared with adjacent non‐cancerous tissues or controls, and its expression was correlated with the overall survival, cancer recurrence and distant metastasis. In the HCC mouse model, liver‐to‐body weight ratio was of the Ccl5−/− group were higher than that of the WT group. Moreover, compared with the WT mice, the number of B cells in the tumor tissue of the Ccl5−/− mice was lower, while there were no significant differences in the other immune cell populations. Furthermore, serum IgM level of the Ccl5−/− mice was significantly lower than that of the WT mice. Conclusion CCL5 expression is decreased in HCC tissues. CCL5 deficiency reduces B cell recruitment and decreases IgM secretion in HCC, potentially leading to tumor progression. CCL5 expression was low in hepatocellular carcinoma (HCC) tissue and peripheral blood of the HCC patients, and its expression was correlated with the overall survival, recurrence and metastasis of the tumor. Deficiency of CCL5 in hepatocellular carcinoma accelerates tumor progression by decreasing B‐cell recruitment and IgM secretion.</description><subject>B cell recruitment</subject><subject>Body weight</subject><subject>chemokine CCL5</subject><subject>Chemokines</subject><subject>Diethylnitrosamine</subject><subject>disease progression</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Hepatocellular carcinoma</subject><subject>hepatocellular carcinomaimmunoglobulin M</subject><subject>Immunoglobulin M</subject><subject>Immunohistochemistry</subject><subject>Ligands</subject><subject>Liver cancer</subject><subject>Lymphocytes B</subject><subject>Metastases</subject><subject>Microenvironments</subject><subject>Peripheral blood</subject><subject>Polymerase chain reaction</subject><issn>1751-2972</issn><issn>1751-2980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNqFkctqGzEUhofSQtOk624F3XTjRJeRNF4249zAkE26FrJ0ZCudkRxphuJdHiHkEfMk0dTBi0KJNrp93-GHv6q-EXxKyjojkpMZnTflSudz-aE6Orx8PJwl_Vx9yfkeYy5kI46q5_bl8alFZgN9_O0DoA1s9RANdN3Y6YSMTsaH2GvUx8E71Pm1DhbxYllw3ngIZoe2KZZvyP-3C7FOkLOPAa12SDsHZvBhjc7RRKMEJo1-6CEMJ9Unp7sMX9_24-rX5cVdez1b3l7dtD-XM8PqRs6oAy3AGpCONUKsTGMd0RZWwK0UXGOpWc1rYQmTtiEWM025lK4xVDtYWXZc_djPLdkeRsiD6n2ewugAccyKcipITRnDBf3-D3ofxxRKukJxTCTDtSjU2Z4yKeacwKlt8r1OO0WwmjpSUwtqakT97agYfG_88R3s3sNVu1jsvVf56pj7</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Li, Xiang</creator><creator>Han, Qiu Cheng</creator><creator>Yu, Chang</creator><creator>Luo, Yi Chun</creator><creator>Wang, Fang</creator><creator>Sun, Xue Hua</creator><creator>Gao, Yue Qiu</creator><creator>Tan, Wei Feng</creator><creator>Xia, Qiang</creator><general>Wiley Publishing Asia Pty Ltd</general><general>Wiley Subscription Services, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7644-1994</orcidid></search><sort><creationdate>202107</creationdate><title>C‐C chemokine hepatocellular carcinoma motif ligand 5‐deficiency promotes hepatocellular carcinoma progression by affecting B cell recruitment</title><author>Li, Xiang ; Han, Qiu Cheng ; Yu, Chang ; Luo, Yi Chun ; Wang, Fang ; Sun, Xue Hua ; Gao, Yue Qiu ; Tan, Wei Feng ; Xia, Qiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3487-2fea6edce7f3866bc8df1adebe5d765a07a34546d137d81d03a2577f8c2afebd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>B cell recruitment</topic><topic>Body weight</topic><topic>chemokine CCL5</topic><topic>Chemokines</topic><topic>Diethylnitrosamine</topic><topic>disease progression</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Hepatocellular carcinoma</topic><topic>hepatocellular carcinomaimmunoglobulin M</topic><topic>Immunoglobulin M</topic><topic>Immunohistochemistry</topic><topic>Ligands</topic><topic>Liver cancer</topic><topic>Lymphocytes B</topic><topic>Metastases</topic><topic>Microenvironments</topic><topic>Peripheral blood</topic><topic>Polymerase chain reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xiang</creatorcontrib><creatorcontrib>Han, Qiu Cheng</creatorcontrib><creatorcontrib>Yu, Chang</creatorcontrib><creatorcontrib>Luo, Yi Chun</creatorcontrib><creatorcontrib>Wang, Fang</creatorcontrib><creatorcontrib>Sun, Xue Hua</creatorcontrib><creatorcontrib>Gao, Yue Qiu</creatorcontrib><creatorcontrib>Tan, Wei Feng</creatorcontrib><creatorcontrib>Xia, Qiang</creatorcontrib><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of digestive diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xiang</au><au>Han, Qiu Cheng</au><au>Yu, Chang</au><au>Luo, Yi Chun</au><au>Wang, Fang</au><au>Sun, Xue Hua</au><au>Gao, Yue Qiu</au><au>Tan, Wei Feng</au><au>Xia, Qiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C‐C chemokine hepatocellular carcinoma motif ligand 5‐deficiency promotes hepatocellular carcinoma progression by affecting B cell recruitment</atitle><jtitle>Journal of digestive diseases</jtitle><date>2021-07</date><risdate>2021</risdate><volume>22</volume><issue>7</issue><spage>433</spage><epage>441</epage><pages>433-441</pages><issn>1751-2972</issn><eissn>1751-2980</eissn><abstract>Objective To evaluate the expression of C‐C motif chemokine ligand 5 (CCL5) in hepatocellular carcinoma (HCC) and to explore its role in regulating the immune microenvironment and the related mechanism in tumor immunity. Methods The mRNA expression level of CCL5 in HCC and adjacent non‐cancerous tissues was measured by quantitative polymerase chain reaction and the protein expression was examined by immunohistochemistry. Serum CCL5 expression was measured by an enzyme‐linked immunosorbent assay (ELISA). C57BL/6 wild‐type (WT) and Ccl5‐knockout (Ccl5−/−) mice were utilized to conduct the diethylnitrosamine‐induced HCC model. The immune cell population was determined by flow cytometry, and peripheral serum immunoglobulin M (IgM) level was quantified by ELISA. Results CCL5 expression was low in HCC tissue and peripheral blood compared with adjacent non‐cancerous tissues or controls, and its expression was correlated with the overall survival, cancer recurrence and distant metastasis. In the HCC mouse model, liver‐to‐body weight ratio was of the Ccl5−/− group were higher than that of the WT group. Moreover, compared with the WT mice, the number of B cells in the tumor tissue of the Ccl5−/− mice was lower, while there were no significant differences in the other immune cell populations. Furthermore, serum IgM level of the Ccl5−/− mice was significantly lower than that of the WT mice. Conclusion CCL5 expression is decreased in HCC tissues. CCL5 deficiency reduces B cell recruitment and decreases IgM secretion in HCC, potentially leading to tumor progression. CCL5 expression was low in hepatocellular carcinoma (HCC) tissue and peripheral blood of the HCC patients, and its expression was correlated with the overall survival, recurrence and metastasis of the tumor. Deficiency of CCL5 in hepatocellular carcinoma accelerates tumor progression by decreasing B‐cell recruitment and IgM secretion.</abstract><cop>Melbourne</cop><pub>Wiley Publishing Asia Pty Ltd</pub><doi>10.1111/1751-2980.12997</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-7644-1994</orcidid></addata></record>
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subjects B cell recruitment
Body weight
chemokine CCL5
Chemokines
Diethylnitrosamine
disease progression
Enzyme-linked immunosorbent assay
Flow cytometry
Gene expression
Hepatocellular carcinoma
hepatocellular carcinomaimmunoglobulin M
Immunoglobulin M
Immunohistochemistry
Ligands
Liver cancer
Lymphocytes B
Metastases
Microenvironments
Peripheral blood
Polymerase chain reaction
title C‐C chemokine hepatocellular carcinoma motif ligand 5‐deficiency promotes hepatocellular carcinoma progression by affecting B cell recruitment
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