The role of vesicular overexpressed in cancer pro-survival protein 1 in hepatocellular carcinoma proliferation
BACKGROUND: Recently, hepatocellular carcinoma (HCC) has been ranked as the second leading cause of cancer-associated death. However, the underlying molecular mechanisms of HCC progression remain unclear. Vesicular overexpressed in cancer pro-survival protein 1 (VOPP1) could be upregulated in a quan...
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| Veröffentlicht in: | Cancer biomarkers : section A of Disease markers 2020-01, Vol.28 (1), p.9-20 |
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| container_title | Cancer biomarkers : section A of Disease markers |
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| creator | Fang, Zheping Wu, Linjun Dai, Haojiang Hu, Peng Wang, Binfeng Han, Qiuyue Xu, Yongfu Lv, Shangdong Zhu, Yu Gan, Meifu Zhou, Weijie Zhang, Wenlong |
| description | BACKGROUND:
Recently, hepatocellular carcinoma (HCC) has been ranked as the second leading cause of cancer-associated death. However, the underlying molecular mechanisms of HCC progression remain unclear. Vesicular overexpressed in cancer pro-survival protein 1 (VOPP1) could be upregulated in a quantity of human cancers, including squamous cell carcinoma (SCC), gastric cancer, and glioblastoma. However, the precise functional mechanism of VOPP1 in HCC remains poorly understood. The present study aimed to investigate the role of VOPP1 in HCC proliferation.
METHODS:
Immunohistochemistry (IHC), Western blot and Reverse-transcription polymerase chain reaction (RT-PCR) were used to analyze the protein and mRNA expressions of VOPP1, mitogen-activated protein kinase (MAPK) 14, ribosomal protein S6 kinase
β
1 (RPS6KB1), cylindromatosis (CYLD) and Twist family bHLH transcription factor 1 (TWIST1). The cell proliferation and apoptosis were tested using Celigo cell imaging analyzer and annexin V-APC apoptosis detection kit respectively. Colony formation and tumor xenograft assays were performed to understand their roles in tumorigenicity.
RESULTS:
The expression of VOPP1 in HCC samples was higher than that in adjacent noncancerous tissues by immunohistochemistry. In addition, the down-regulation of VOPP1 using shRNA inhibited cell proliferation and tumour growth, and induced cell apoptosis in vitro and in vivo. Furthermore, VOPP1 silencing increased the expression of MAPK14 and RPS6KB1, indicating that the MAPK and mTOR signalling pathways might be involved in VOPP1-mediated cancer cell proliferation.
CONCLUSION:
The present data indicate that VOPP1 may play an important role in the progression of HCC by targeting the MAPK and mTOR signalling pathways, and that VOPP1 may potentially be a candidate as a novel molecular target for HCC therapy. |
| doi_str_mv | 10.3233/CBM-190574 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_AFRWT</sourceid><recordid>TN_cdi_proquest_miscellaneous_2362065657</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.3233_CBM-190574</sage_id><sourcerecordid>2362065657</sourcerecordid><originalsourceid>FETCH-LOGICAL-c388t-d3980a3654b6172a9aa640e8c205d6c1d78f1aea77dec9833a5afffb894e457b3</originalsourceid><addsrcrecordid>eNpt0UtLxDAQB_Agiq6rFz-AFDwoQjWPpkmOuvgCxct6LrPpVLt0mzVpF_32pq4PEE95_fjPkCHkgNEzwYU4n1w-pMxQqbINMmJayVRLwzfjPl6llEmxQ3ZDmFOaCcbNNtkRnGohcz0i7fQFE-8aTFyVrDDUtm_AJ26FHt-WHkPAMqnbxEJr0SdL79LQ-1W9gmY4dBjf2ABecAmds9g0nwEWvK1bt4BBNXWFHrratXtkq4Im4P7XOiZP11fTyW16_3hzN7m4T63QuktLYTQFkctsljPFwQDkGUVtOZVlblmpdMUAQakSrdFCgISqqmbaZJhJNRNjcrLOjdVfewxdsajD0By06PpQcJFzmstcqkiP_tC5630bu4vKGKO14jqq07Wy3oXgsSqWvl6Afy8YLYYpFHEKxXoKER9-RfazBZY_9PvbIzhegwDP-Fvvn6gPKOSPfQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2399988728</pqid></control><display><type>article</type><title>The role of vesicular overexpressed in cancer pro-survival protein 1 in hepatocellular carcinoma proliferation</title><source>Sage Journals GOLD Open Access 2024</source><creator>Fang, Zheping ; Wu, Linjun ; Dai, Haojiang ; Hu, Peng ; Wang, Binfeng ; Han, Qiuyue ; Xu, Yongfu ; Lv, Shangdong ; Zhu, Yu ; Gan, Meifu ; Zhou, Weijie ; Zhang, Wenlong</creator><creatorcontrib>Fang, Zheping ; Wu, Linjun ; Dai, Haojiang ; Hu, Peng ; Wang, Binfeng ; Han, Qiuyue ; Xu, Yongfu ; Lv, Shangdong ; Zhu, Yu ; Gan, Meifu ; Zhou, Weijie ; Zhang, Wenlong</creatorcontrib><description>BACKGROUND:
Recently, hepatocellular carcinoma (HCC) has been ranked as the second leading cause of cancer-associated death. However, the underlying molecular mechanisms of HCC progression remain unclear. Vesicular overexpressed in cancer pro-survival protein 1 (VOPP1) could be upregulated in a quantity of human cancers, including squamous cell carcinoma (SCC), gastric cancer, and glioblastoma. However, the precise functional mechanism of VOPP1 in HCC remains poorly understood. The present study aimed to investigate the role of VOPP1 in HCC proliferation.
METHODS:
Immunohistochemistry (IHC), Western blot and Reverse-transcription polymerase chain reaction (RT-PCR) were used to analyze the protein and mRNA expressions of VOPP1, mitogen-activated protein kinase (MAPK) 14, ribosomal protein S6 kinase
β
1 (RPS6KB1), cylindromatosis (CYLD) and Twist family bHLH transcription factor 1 (TWIST1). The cell proliferation and apoptosis were tested using Celigo cell imaging analyzer and annexin V-APC apoptosis detection kit respectively. Colony formation and tumor xenograft assays were performed to understand their roles in tumorigenicity.
RESULTS:
The expression of VOPP1 in HCC samples was higher than that in adjacent noncancerous tissues by immunohistochemistry. In addition, the down-regulation of VOPP1 using shRNA inhibited cell proliferation and tumour growth, and induced cell apoptosis in vitro and in vivo. Furthermore, VOPP1 silencing increased the expression of MAPK14 and RPS6KB1, indicating that the MAPK and mTOR signalling pathways might be involved in VOPP1-mediated cancer cell proliferation.
CONCLUSION:
The present data indicate that VOPP1 may play an important role in the progression of HCC by targeting the MAPK and mTOR signalling pathways, and that VOPP1 may potentially be a candidate as a novel molecular target for HCC therapy.</description><identifier>ISSN: 1574-0153</identifier><identifier>EISSN: 1875-8592</identifier><identifier>DOI: 10.3233/CBM-190574</identifier><identifier>PMID: 32083568</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adenomatous polyposis coli ; Adult ; Aged ; Annexin V ; Apoptosis ; Cancer ; Carcinoma, Hepatocellular - genetics ; Cell growth ; Cell Proliferation ; Female ; Gastric cancer ; Glioblastoma ; Helix-loop-helix proteins (basic) ; Hepatocellular carcinoma ; Humans ; Immunohistochemistry ; Kinases ; Liver cancer ; Liver Neoplasms - genetics ; Male ; MAP kinase ; Middle Aged ; Molecular modelling ; Oncogene Proteins - genetics ; Polymerase chain reaction ; Protein kinase ; Proteins ; Ribosomal protein S6 ; Ribosomal protein S6 kinase ; Signal transduction ; Signaling ; Squamous cell carcinoma ; Survival ; TOR protein ; Transcription Factors - metabolism ; Tumorigenicity ; Tumors ; Xenografts ; Xenotransplantation</subject><ispartof>Cancer biomarkers : section A of Disease markers, 2020-01, Vol.28 (1), p.9-20</ispartof><rights>2020 – IOS Press and the authors. All rights reserved</rights><rights>Copyright IOS Press BV 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-d3980a3654b6172a9aa640e8c205d6c1d78f1aea77dec9833a5afffb894e457b3</citedby><cites>FETCH-LOGICAL-c388t-d3980a3654b6172a9aa640e8c205d6c1d78f1aea77dec9833a5afffb894e457b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.3233/CBM-190574$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.3233/CBM-190574$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21945,27830,27901,27902,44921,45309</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.3233/CBM-190574?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32083568$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fang, Zheping</creatorcontrib><creatorcontrib>Wu, Linjun</creatorcontrib><creatorcontrib>Dai, Haojiang</creatorcontrib><creatorcontrib>Hu, Peng</creatorcontrib><creatorcontrib>Wang, Binfeng</creatorcontrib><creatorcontrib>Han, Qiuyue</creatorcontrib><creatorcontrib>Xu, Yongfu</creatorcontrib><creatorcontrib>Lv, Shangdong</creatorcontrib><creatorcontrib>Zhu, Yu</creatorcontrib><creatorcontrib>Gan, Meifu</creatorcontrib><creatorcontrib>Zhou, Weijie</creatorcontrib><creatorcontrib>Zhang, Wenlong</creatorcontrib><title>The role of vesicular overexpressed in cancer pro-survival protein 1 in hepatocellular carcinoma proliferation</title><title>Cancer biomarkers : section A of Disease markers</title><addtitle>Cancer Biomark</addtitle><description>BACKGROUND:
Recently, hepatocellular carcinoma (HCC) has been ranked as the second leading cause of cancer-associated death. However, the underlying molecular mechanisms of HCC progression remain unclear. Vesicular overexpressed in cancer pro-survival protein 1 (VOPP1) could be upregulated in a quantity of human cancers, including squamous cell carcinoma (SCC), gastric cancer, and glioblastoma. However, the precise functional mechanism of VOPP1 in HCC remains poorly understood. The present study aimed to investigate the role of VOPP1 in HCC proliferation.
METHODS:
Immunohistochemistry (IHC), Western blot and Reverse-transcription polymerase chain reaction (RT-PCR) were used to analyze the protein and mRNA expressions of VOPP1, mitogen-activated protein kinase (MAPK) 14, ribosomal protein S6 kinase
β
1 (RPS6KB1), cylindromatosis (CYLD) and Twist family bHLH transcription factor 1 (TWIST1). The cell proliferation and apoptosis were tested using Celigo cell imaging analyzer and annexin V-APC apoptosis detection kit respectively. Colony formation and tumor xenograft assays were performed to understand their roles in tumorigenicity.
RESULTS:
The expression of VOPP1 in HCC samples was higher than that in adjacent noncancerous tissues by immunohistochemistry. In addition, the down-regulation of VOPP1 using shRNA inhibited cell proliferation and tumour growth, and induced cell apoptosis in vitro and in vivo. Furthermore, VOPP1 silencing increased the expression of MAPK14 and RPS6KB1, indicating that the MAPK and mTOR signalling pathways might be involved in VOPP1-mediated cancer cell proliferation.
CONCLUSION:
The present data indicate that VOPP1 may play an important role in the progression of HCC by targeting the MAPK and mTOR signalling pathways, and that VOPP1 may potentially be a candidate as a novel molecular target for HCC therapy.</description><subject>Adenomatous polyposis coli</subject><subject>Adult</subject><subject>Aged</subject><subject>Annexin V</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Glioblastoma</subject><subject>Helix-loop-helix proteins (basic)</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Male</subject><subject>MAP kinase</subject><subject>Middle Aged</subject><subject>Molecular modelling</subject><subject>Oncogene Proteins - genetics</subject><subject>Polymerase chain reaction</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Ribosomal protein S6</subject><subject>Ribosomal protein S6 kinase</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Squamous cell carcinoma</subject><subject>Survival</subject><subject>TOR protein</subject><subject>Transcription Factors - metabolism</subject><subject>Tumorigenicity</subject><subject>Tumors</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>1574-0153</issn><issn>1875-8592</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0UtLxDAQB_Agiq6rFz-AFDwoQjWPpkmOuvgCxct6LrPpVLt0mzVpF_32pq4PEE95_fjPkCHkgNEzwYU4n1w-pMxQqbINMmJayVRLwzfjPl6llEmxQ3ZDmFOaCcbNNtkRnGohcz0i7fQFE-8aTFyVrDDUtm_AJ26FHt-WHkPAMqnbxEJr0SdL79LQ-1W9gmY4dBjf2ABecAmds9g0nwEWvK1bt4BBNXWFHrratXtkq4Im4P7XOiZP11fTyW16_3hzN7m4T63QuktLYTQFkctsljPFwQDkGUVtOZVlblmpdMUAQakSrdFCgISqqmbaZJhJNRNjcrLOjdVfewxdsajD0By06PpQcJFzmstcqkiP_tC5630bu4vKGKO14jqq07Wy3oXgsSqWvl6Afy8YLYYpFHEKxXoKER9-RfazBZY_9PvbIzhegwDP-Fvvn6gPKOSPfQ</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Fang, Zheping</creator><creator>Wu, Linjun</creator><creator>Dai, Haojiang</creator><creator>Hu, Peng</creator><creator>Wang, Binfeng</creator><creator>Han, Qiuyue</creator><creator>Xu, Yongfu</creator><creator>Lv, Shangdong</creator><creator>Zhu, Yu</creator><creator>Gan, Meifu</creator><creator>Zhou, Weijie</creator><creator>Zhang, Wenlong</creator><general>SAGE Publications</general><general>IOS Press BV</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>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20200101</creationdate><title>The role of vesicular overexpressed in cancer pro-survival protein 1 in hepatocellular carcinoma proliferation</title><author>Fang, Zheping ; Wu, Linjun ; Dai, Haojiang ; Hu, Peng ; Wang, Binfeng ; Han, Qiuyue ; Xu, Yongfu ; Lv, Shangdong ; Zhu, Yu ; Gan, Meifu ; Zhou, Weijie ; Zhang, Wenlong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-d3980a3654b6172a9aa640e8c205d6c1d78f1aea77dec9833a5afffb894e457b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenomatous polyposis coli</topic><topic>Adult</topic><topic>Aged</topic><topic>Annexin V</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Glioblastoma</topic><topic>Helix-loop-helix proteins (basic)</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Male</topic><topic>MAP kinase</topic><topic>Middle Aged</topic><topic>Molecular modelling</topic><topic>Oncogene Proteins - genetics</topic><topic>Polymerase chain reaction</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Ribosomal protein S6</topic><topic>Ribosomal protein S6 kinase</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Squamous cell carcinoma</topic><topic>Survival</topic><topic>TOR protein</topic><topic>Transcription Factors - metabolism</topic><topic>Tumorigenicity</topic><topic>Tumors</topic><topic>Xenografts</topic><topic>Xenotransplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fang, Zheping</creatorcontrib><creatorcontrib>Wu, Linjun</creatorcontrib><creatorcontrib>Dai, Haojiang</creatorcontrib><creatorcontrib>Hu, Peng</creatorcontrib><creatorcontrib>Wang, Binfeng</creatorcontrib><creatorcontrib>Han, Qiuyue</creatorcontrib><creatorcontrib>Xu, Yongfu</creatorcontrib><creatorcontrib>Lv, Shangdong</creatorcontrib><creatorcontrib>Zhu, Yu</creatorcontrib><creatorcontrib>Gan, Meifu</creatorcontrib><creatorcontrib>Zhou, Weijie</creatorcontrib><creatorcontrib>Zhang, Wenlong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer biomarkers : section A of Disease markers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Fang, Zheping</au><au>Wu, Linjun</au><au>Dai, Haojiang</au><au>Hu, Peng</au><au>Wang, Binfeng</au><au>Han, Qiuyue</au><au>Xu, Yongfu</au><au>Lv, Shangdong</au><au>Zhu, Yu</au><au>Gan, Meifu</au><au>Zhou, Weijie</au><au>Zhang, Wenlong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of vesicular overexpressed in cancer pro-survival protein 1 in hepatocellular carcinoma proliferation</atitle><jtitle>Cancer biomarkers : section A of Disease markers</jtitle><addtitle>Cancer Biomark</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>28</volume><issue>1</issue><spage>9</spage><epage>20</epage><pages>9-20</pages><issn>1574-0153</issn><eissn>1875-8592</eissn><abstract>BACKGROUND:
Recently, hepatocellular carcinoma (HCC) has been ranked as the second leading cause of cancer-associated death. However, the underlying molecular mechanisms of HCC progression remain unclear. Vesicular overexpressed in cancer pro-survival protein 1 (VOPP1) could be upregulated in a quantity of human cancers, including squamous cell carcinoma (SCC), gastric cancer, and glioblastoma. However, the precise functional mechanism of VOPP1 in HCC remains poorly understood. The present study aimed to investigate the role of VOPP1 in HCC proliferation.
METHODS:
Immunohistochemistry (IHC), Western blot and Reverse-transcription polymerase chain reaction (RT-PCR) were used to analyze the protein and mRNA expressions of VOPP1, mitogen-activated protein kinase (MAPK) 14, ribosomal protein S6 kinase
β
1 (RPS6KB1), cylindromatosis (CYLD) and Twist family bHLH transcription factor 1 (TWIST1). The cell proliferation and apoptosis were tested using Celigo cell imaging analyzer and annexin V-APC apoptosis detection kit respectively. Colony formation and tumor xenograft assays were performed to understand their roles in tumorigenicity.
RESULTS:
The expression of VOPP1 in HCC samples was higher than that in adjacent noncancerous tissues by immunohistochemistry. In addition, the down-regulation of VOPP1 using shRNA inhibited cell proliferation and tumour growth, and induced cell apoptosis in vitro and in vivo. Furthermore, VOPP1 silencing increased the expression of MAPK14 and RPS6KB1, indicating that the MAPK and mTOR signalling pathways might be involved in VOPP1-mediated cancer cell proliferation.
CONCLUSION:
The present data indicate that VOPP1 may play an important role in the progression of HCC by targeting the MAPK and mTOR signalling pathways, and that VOPP1 may potentially be a candidate as a novel molecular target for HCC therapy.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>32083568</pmid><doi>10.3233/CBM-190574</doi><tpages>12</tpages></addata></record> |
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| source | Sage Journals GOLD Open Access 2024 |
| subjects | Adenomatous polyposis coli Adult Aged Annexin V Apoptosis Cancer Carcinoma, Hepatocellular - genetics Cell growth Cell Proliferation Female Gastric cancer Glioblastoma Helix-loop-helix proteins (basic) Hepatocellular carcinoma Humans Immunohistochemistry Kinases Liver cancer Liver Neoplasms - genetics Male MAP kinase Middle Aged Molecular modelling Oncogene Proteins - genetics Polymerase chain reaction Protein kinase Proteins Ribosomal protein S6 Ribosomal protein S6 kinase Signal transduction Signaling Squamous cell carcinoma Survival TOR protein Transcription Factors - metabolism Tumorigenicity Tumors Xenografts Xenotransplantation |
| title | The role of vesicular overexpressed in cancer pro-survival protein 1 in hepatocellular carcinoma proliferation |
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