Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling
Postsurgical recurrence within 2 years is the major cause of poor survival of hepatocellular carcinoma (HCC) patients. However, the molecular mechanism underlying HCC recurrence remains unclear. Here, we distinguish the function and mechanism of Sec62 in promoting HCC recurrence. The correlation bet...
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| Veröffentlicht in: | Oncogenesis (New York, NY) NY), 2019-12, Vol.8 (12), p.74-9, Article 74 |
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| creator | Du, Juan Zhao, Zhihao Zhao, Hetong Liu, Dong Liu, Hui Chen, Jun Cheng, Binbin Zhai, Xiaofeng Yin, Zifei Zhang, Yani Ling, Changquan |
| description | Postsurgical recurrence within 2 years is the major cause of poor survival of hepatocellular carcinoma (HCC) patients. However, the molecular mechanism underlying HCC recurrence remains unclear. Here, we distinguish the function and mechanism of Sec62 in promoting HCC recurrence. The correlation between Sec62 and early recurrence was demonstrated in 60 HCC samples from a prospective study. HCC cells with Sec62 knockdown (Sec62
KD
) or overexpression (Sec62
OE
) were used to determine the potential of Sec62 in cell migration in vitro. Microarray analysis comparing Sec62
KD
or Sec62
OE
to their control counterparts was used to explore the mechanisms of Sec62-induced recurrence. A luciferase-labelled orthotopic nude mouse model of HCC with Sec62
KD
or Sec62
OE
was used to validate the potential of Sec62 in early HCC recurrence in vivo. We found that high expression of Sec62 was positively correlated with surgical recurrence in clinical HCC samples. Multivariate analysis revealed that Sec62 was an independent prognostic factor for early recurrence in postoperative HCC patients. Moreover, Sec62 promoted migration and invasion of HCC cells in vitro and postsurgical recurrence in vivo. Mechanically, integrinα/CAV1 signalling was identified as one of the targets of Sec62 in cell movement. Overexpression of integrin α partially rescued the Sec62 knockdown-induced inhibition of cell migration. Sec62 is a potentially prognostic factor for early recurrence in postoperative HCC patients and promotes HCC metastasis through integrinα/CAV1 signalling. Sec62 might be an attractive drug target for combating HCC postsurgical recurrence. |
| doi_str_mv | 10.1038/s41389-019-0183-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6904485</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2323445120</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-baff4282d5bc531dd1323bc45f3d1965dc32e8766ee4f39c3bd8178450bd13fc3</originalsourceid><addsrcrecordid>eNp1kc9qFTEYxYMottQ-gBsJuHEzNv9vZiOUS6tCwYV_tiGT-WZuykxyTTKFPpYv4jM14621CgZCAuf3neRwEHpJyVtKuD7LgnLdNoSuW_NGPUHHjMpN0xImnj66H6HTnK9JXVJRJeVzdMSpZkxJdYz8Z3CK4X2KcyyQMdg03eIEbkkJggMcB7yDvS3RwTQtk03Y2eR8iLPFZZfiMu6wdcXf2OLDiH0oMCYffv44255_ozj7MdhpqtIL9GywU4bT-_MEfb28-LL90Fx9ev9xe37VOLEhpensMAimWS87Jznte8oZ75yQA-9pq2TvOAO9UQpADLx1vOs13WghSVfRwfET9O7gu1-6GXoHoSQ7mX3ys023Jlpv_laC35kx3hjVEiG0rAZv7g1S_L5ALmb2eU1vA8QlG8aZaCkVLano63_Q67ikGvgXxYWQlK0UPVAuxZwTDA-focSsXZpDl6Z2adYujaozrx6neJj43VwF2AHIVQojpD9P_9_1Di3_rFU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2323445120</pqid></control><display><type>article</type><title>Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling</title><source>Nature Free</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><source>Springer Nature OA Free Journals</source><creator>Du, Juan ; Zhao, Zhihao ; Zhao, Hetong ; Liu, Dong ; Liu, Hui ; Chen, Jun ; Cheng, Binbin ; Zhai, Xiaofeng ; Yin, Zifei ; Zhang, Yani ; Ling, Changquan</creator><creatorcontrib>Du, Juan ; Zhao, Zhihao ; Zhao, Hetong ; Liu, Dong ; Liu, Hui ; Chen, Jun ; Cheng, Binbin ; Zhai, Xiaofeng ; Yin, Zifei ; Zhang, Yani ; Ling, Changquan</creatorcontrib><description>Postsurgical recurrence within 2 years is the major cause of poor survival of hepatocellular carcinoma (HCC) patients. However, the molecular mechanism underlying HCC recurrence remains unclear. Here, we distinguish the function and mechanism of Sec62 in promoting HCC recurrence. The correlation between Sec62 and early recurrence was demonstrated in 60 HCC samples from a prospective study. HCC cells with Sec62 knockdown (Sec62
KD
) or overexpression (Sec62
OE
) were used to determine the potential of Sec62 in cell migration in vitro. Microarray analysis comparing Sec62
KD
or Sec62
OE
to their control counterparts was used to explore the mechanisms of Sec62-induced recurrence. A luciferase-labelled orthotopic nude mouse model of HCC with Sec62
KD
or Sec62
OE
was used to validate the potential of Sec62 in early HCC recurrence in vivo. We found that high expression of Sec62 was positively correlated with surgical recurrence in clinical HCC samples. Multivariate analysis revealed that Sec62 was an independent prognostic factor for early recurrence in postoperative HCC patients. Moreover, Sec62 promoted migration and invasion of HCC cells in vitro and postsurgical recurrence in vivo. Mechanically, integrinα/CAV1 signalling was identified as one of the targets of Sec62 in cell movement. Overexpression of integrin α partially rescued the Sec62 knockdown-induced inhibition of cell migration. Sec62 is a potentially prognostic factor for early recurrence in postoperative HCC patients and promotes HCC metastasis through integrinα/CAV1 signalling. Sec62 might be an attractive drug target for combating HCC postsurgical recurrence.</description><identifier>ISSN: 2157-9024</identifier><identifier>EISSN: 2157-9024</identifier><identifier>DOI: 10.1038/s41389-019-0183-6</identifier><identifier>PMID: 31822656</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/89 ; 38/61 ; 631/67/1857 ; 631/67/322 ; 64/60 ; Apoptosis ; Calcium channels (voltage-gated) ; Cell adhesion & migration ; Cell Biology ; Hepatocellular carcinoma ; Human Genetics ; Internal Medicine ; Liver cancer ; Medicine ; Medicine & Public Health ; Oncology</subject><ispartof>Oncogenesis (New York, NY), 2019-12, Vol.8 (12), p.74-9, Article 74</ispartof><rights>The Author(s) 2019</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-baff4282d5bc531dd1323bc45f3d1965dc32e8766ee4f39c3bd8178450bd13fc3</citedby><cites>FETCH-LOGICAL-c470t-baff4282d5bc531dd1323bc45f3d1965dc32e8766ee4f39c3bd8178450bd13fc3</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/PMC6904485/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904485/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31822656$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Juan</creatorcontrib><creatorcontrib>Zhao, Zhihao</creatorcontrib><creatorcontrib>Zhao, Hetong</creatorcontrib><creatorcontrib>Liu, Dong</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Cheng, Binbin</creatorcontrib><creatorcontrib>Zhai, Xiaofeng</creatorcontrib><creatorcontrib>Yin, Zifei</creatorcontrib><creatorcontrib>Zhang, Yani</creatorcontrib><creatorcontrib>Ling, Changquan</creatorcontrib><title>Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling</title><title>Oncogenesis (New York, NY)</title><addtitle>Oncogenesis</addtitle><addtitle>Oncogenesis</addtitle><description>Postsurgical recurrence within 2 years is the major cause of poor survival of hepatocellular carcinoma (HCC) patients. However, the molecular mechanism underlying HCC recurrence remains unclear. Here, we distinguish the function and mechanism of Sec62 in promoting HCC recurrence. The correlation between Sec62 and early recurrence was demonstrated in 60 HCC samples from a prospective study. HCC cells with Sec62 knockdown (Sec62
KD
) or overexpression (Sec62
OE
) were used to determine the potential of Sec62 in cell migration in vitro. Microarray analysis comparing Sec62
KD
or Sec62
OE
to their control counterparts was used to explore the mechanisms of Sec62-induced recurrence. A luciferase-labelled orthotopic nude mouse model of HCC with Sec62
KD
or Sec62
OE
was used to validate the potential of Sec62 in early HCC recurrence in vivo. We found that high expression of Sec62 was positively correlated with surgical recurrence in clinical HCC samples. Multivariate analysis revealed that Sec62 was an independent prognostic factor for early recurrence in postoperative HCC patients. Moreover, Sec62 promoted migration and invasion of HCC cells in vitro and postsurgical recurrence in vivo. Mechanically, integrinα/CAV1 signalling was identified as one of the targets of Sec62 in cell movement. Overexpression of integrin α partially rescued the Sec62 knockdown-induced inhibition of cell migration. Sec62 is a potentially prognostic factor for early recurrence in postoperative HCC patients and promotes HCC metastasis through integrinα/CAV1 signalling. Sec62 might be an attractive drug target for combating HCC postsurgical recurrence.</description><subject>13/109</subject><subject>13/89</subject><subject>38/61</subject><subject>631/67/1857</subject><subject>631/67/322</subject><subject>64/60</subject><subject>Apoptosis</subject><subject>Calcium channels (voltage-gated)</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Hepatocellular carcinoma</subject><subject>Human Genetics</subject><subject>Internal Medicine</subject><subject>Liver cancer</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><issn>2157-9024</issn><issn>2157-9024</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc9qFTEYxYMottQ-gBsJuHEzNv9vZiOUS6tCwYV_tiGT-WZuykxyTTKFPpYv4jM14621CgZCAuf3neRwEHpJyVtKuD7LgnLdNoSuW_NGPUHHjMpN0xImnj66H6HTnK9JXVJRJeVzdMSpZkxJdYz8Z3CK4X2KcyyQMdg03eIEbkkJggMcB7yDvS3RwTQtk03Y2eR8iLPFZZfiMu6wdcXf2OLDiH0oMCYffv44255_ozj7MdhpqtIL9GywU4bT-_MEfb28-LL90Fx9ev9xe37VOLEhpensMAimWS87Jznte8oZ75yQA-9pq2TvOAO9UQpADLx1vOs13WghSVfRwfET9O7gu1-6GXoHoSQ7mX3ys023Jlpv_laC35kx3hjVEiG0rAZv7g1S_L5ALmb2eU1vA8QlG8aZaCkVLano63_Q67ikGvgXxYWQlK0UPVAuxZwTDA-focSsXZpDl6Z2adYujaozrx6neJj43VwF2AHIVQojpD9P_9_1Di3_rFU</recordid><startdate>20191210</startdate><enddate>20191210</enddate><creator>Du, Juan</creator><creator>Zhao, Zhihao</creator><creator>Zhao, Hetong</creator><creator>Liu, Dong</creator><creator>Liu, Hui</creator><creator>Chen, Jun</creator><creator>Cheng, Binbin</creator><creator>Zhai, Xiaofeng</creator><creator>Yin, Zifei</creator><creator>Zhang, Yani</creator><creator>Ling, Changquan</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20191210</creationdate><title>Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling</title><author>Du, Juan ; Zhao, Zhihao ; Zhao, Hetong ; Liu, Dong ; Liu, Hui ; Chen, Jun ; Cheng, Binbin ; Zhai, Xiaofeng ; Yin, Zifei ; Zhang, Yani ; Ling, Changquan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-baff4282d5bc531dd1323bc45f3d1965dc32e8766ee4f39c3bd8178450bd13fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13/109</topic><topic>13/89</topic><topic>38/61</topic><topic>631/67/1857</topic><topic>631/67/322</topic><topic>64/60</topic><topic>Apoptosis</topic><topic>Calcium channels (voltage-gated)</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Hepatocellular carcinoma</topic><topic>Human Genetics</topic><topic>Internal Medicine</topic><topic>Liver cancer</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Du, Juan</creatorcontrib><creatorcontrib>Zhao, Zhihao</creatorcontrib><creatorcontrib>Zhao, Hetong</creatorcontrib><creatorcontrib>Liu, Dong</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Cheng, Binbin</creatorcontrib><creatorcontrib>Zhai, Xiaofeng</creatorcontrib><creatorcontrib>Yin, Zifei</creatorcontrib><creatorcontrib>Zhang, Yani</creatorcontrib><creatorcontrib>Ling, Changquan</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogenesis (New York, NY)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Juan</au><au>Zhao, Zhihao</au><au>Zhao, Hetong</au><au>Liu, Dong</au><au>Liu, Hui</au><au>Chen, Jun</au><au>Cheng, Binbin</au><au>Zhai, Xiaofeng</au><au>Yin, Zifei</au><au>Zhang, Yani</au><au>Ling, Changquan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling</atitle><jtitle>Oncogenesis (New York, NY)</jtitle><stitle>Oncogenesis</stitle><addtitle>Oncogenesis</addtitle><date>2019-12-10</date><risdate>2019</risdate><volume>8</volume><issue>12</issue><spage>74</spage><epage>9</epage><pages>74-9</pages><artnum>74</artnum><issn>2157-9024</issn><eissn>2157-9024</eissn><abstract>Postsurgical recurrence within 2 years is the major cause of poor survival of hepatocellular carcinoma (HCC) patients. However, the molecular mechanism underlying HCC recurrence remains unclear. Here, we distinguish the function and mechanism of Sec62 in promoting HCC recurrence. The correlation between Sec62 and early recurrence was demonstrated in 60 HCC samples from a prospective study. HCC cells with Sec62 knockdown (Sec62
KD
) or overexpression (Sec62
OE
) were used to determine the potential of Sec62 in cell migration in vitro. Microarray analysis comparing Sec62
KD
or Sec62
OE
to their control counterparts was used to explore the mechanisms of Sec62-induced recurrence. A luciferase-labelled orthotopic nude mouse model of HCC with Sec62
KD
or Sec62
OE
was used to validate the potential of Sec62 in early HCC recurrence in vivo. We found that high expression of Sec62 was positively correlated with surgical recurrence in clinical HCC samples. Multivariate analysis revealed that Sec62 was an independent prognostic factor for early recurrence in postoperative HCC patients. Moreover, Sec62 promoted migration and invasion of HCC cells in vitro and postsurgical recurrence in vivo. Mechanically, integrinα/CAV1 signalling was identified as one of the targets of Sec62 in cell movement. Overexpression of integrin α partially rescued the Sec62 knockdown-induced inhibition of cell migration. Sec62 is a potentially prognostic factor for early recurrence in postoperative HCC patients and promotes HCC metastasis through integrinα/CAV1 signalling. Sec62 might be an attractive drug target for combating HCC postsurgical recurrence.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31822656</pmid><doi>10.1038/s41389-019-0183-6</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access; Springer Nature OA Free Journals |
| subjects | 13/109 13/89 38/61 631/67/1857 631/67/322 64/60 Apoptosis Calcium channels (voltage-gated) Cell adhesion & migration Cell Biology Hepatocellular carcinoma Human Genetics Internal Medicine Liver cancer Medicine Medicine & Public Health Oncology |
| title | Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling |
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