Co-Upregulation of 14-3-3ζ and P-Akt is Associated with Oncogenesis and Recurrence of Hepatocellular Carcinoma
Background/Aims: 14-3-3ζ is involved in the regulation of PI3K/Akt pathway which is closely associated with carcinogenesis. However, the clinical significance of combined detection of 14-3-3ζ and p-Akt in hepatocellular carcinoma (HCC) remains unclear. Methods: Two-hundred pairs of HCC and adjacent...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.45 (3), p.1097-1107 |
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| creator | Tang, Yufu Wang, Ruoyu Zhang, Yibing Lin, Shenhui Qiao, Na Sun, Zhongyi Cheng, Shuqun Zhou, Wenping |
| description | Background/Aims: 14-3-3ζ is involved in the regulation of PI3K/Akt pathway which is closely associated with carcinogenesis. However, the clinical significance of combined detection of 14-3-3ζ and p-Akt in hepatocellular carcinoma (HCC) remains unclear. Methods: Two-hundred pairs of HCC and adjacent liver specimens were subjected to tissue microarray. The association of 14-3-3ζ and p-Akt levels with the postoperative survival and recurrence in HCC patients was analyzed with univariate and multivariate methods. Moreover, the effects of 14-3-3ζ overexpression on the growth of HCC and the expressions of p-Akt and HIF-1α were assessed in a xenograft mouse model. Results: Elevated levels of 14-3-3ζ and p-Akt were detected in HCC and a positive correlation between the levels of 14-3-3ζ and p-Akt was verified. HCC patients with satellite nodules, microvascular invasion, portal vein tumor thrombosis, poor tumor differentiation and an advanced tumor stage tended to have higher levels of 14-3-3ζ and p-Akt. In addition, the postoperative 3-, 5-, and 7-year overall survival rates in HCC patients with 14-3-3ζ high and p-Akt high were significantly lower compared with those with 14-3-3ζ low and p-Akt low , and the cumulative recurrence rate in HCC patients with 14-3-3ζ high and p-Akt high was significantly higher than that in those with 14-3-3ζ low and p-Akt low . The multivariate Cox proportional hazard analysis indicated that concomitant upregulation of 14-3-3ζ and p-Akt was an independent factor that predicted poor survival and high recurrence in HCC patients. Furthermore, animal experiment showed that overexpression of 14-3-3ζ accelerated the growth of HCC xenograft tumors and induced the expressions of p-Akt and HIF-1α in vivo. Conclusion: Co-upregulation of 14-3-3ζ and p-Akt predicts poor prognosis in patients with HCC, and 14-3-3ζ-induced activation of the Akt signaling pathway contributes to HCC progression. |
| doi_str_mv | 10.1159/000487351 |
| format | Article |
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However, the clinical significance of combined detection of 14-3-3ζ and p-Akt in hepatocellular carcinoma (HCC) remains unclear. Methods: Two-hundred pairs of HCC and adjacent liver specimens were subjected to tissue microarray. The association of 14-3-3ζ and p-Akt levels with the postoperative survival and recurrence in HCC patients was analyzed with univariate and multivariate methods. Moreover, the effects of 14-3-3ζ overexpression on the growth of HCC and the expressions of p-Akt and HIF-1α were assessed in a xenograft mouse model. Results: Elevated levels of 14-3-3ζ and p-Akt were detected in HCC and a positive correlation between the levels of 14-3-3ζ and p-Akt was verified. HCC patients with satellite nodules, microvascular invasion, portal vein tumor thrombosis, poor tumor differentiation and an advanced tumor stage tended to have higher levels of 14-3-3ζ and p-Akt. In addition, the postoperative 3-, 5-, and 7-year overall survival rates in HCC patients with 14-3-3ζ high and p-Akt high were significantly lower compared with those with 14-3-3ζ low and p-Akt low , and the cumulative recurrence rate in HCC patients with 14-3-3ζ high and p-Akt high was significantly higher than that in those with 14-3-3ζ low and p-Akt low . The multivariate Cox proportional hazard analysis indicated that concomitant upregulation of 14-3-3ζ and p-Akt was an independent factor that predicted poor survival and high recurrence in HCC patients. Furthermore, animal experiment showed that overexpression of 14-3-3ζ accelerated the growth of HCC xenograft tumors and induced the expressions of p-Akt and HIF-1α in vivo. Conclusion: Co-upregulation of 14-3-3ζ and p-Akt predicts poor prognosis in patients with HCC, and 14-3-3ζ-induced activation of the Akt signaling pathway contributes to HCC progression.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000487351</identifier><identifier>PMID: 29439255</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>14-3-3 Proteins - genetics ; 14-3-3 Proteins - metabolism ; 14-3-3ζ ; Aged ; Animal research ; Animals ; Apoptosis ; Cancer therapies ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - mortality ; Carcinoma, Hepatocellular - pathology ; Cell cycle ; Cell Line, Tumor ; Female ; Hepatitis ; Hepatitis B e Antigens - blood ; Hepatocellular carcinoma ; Hepatology ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Kinases ; Liver - metabolism ; Liver - pathology ; Liver cancer ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Male ; Medical prognosis ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Original Paper ; P-Akt ; Phosphorylation ; Prognosis ; Proteins ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; Surgery ; Up-Regulation</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.45 (3), p.1097-1107</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-45680f676f1a685bbca282fefcc75647f38dabbc534d2637f6adca94b31ff6643</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2101,27634,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29439255$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Yufu</creatorcontrib><creatorcontrib>Wang, Ruoyu</creatorcontrib><creatorcontrib>Zhang, Yibing</creatorcontrib><creatorcontrib>Lin, Shenhui</creatorcontrib><creatorcontrib>Qiao, Na</creatorcontrib><creatorcontrib>Sun, Zhongyi</creatorcontrib><creatorcontrib>Cheng, Shuqun</creatorcontrib><creatorcontrib>Zhou, Wenping</creatorcontrib><title>Co-Upregulation of 14-3-3ζ and P-Akt is Associated with Oncogenesis and Recurrence of Hepatocellular Carcinoma</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: 14-3-3ζ is involved in the regulation of PI3K/Akt pathway which is closely associated with carcinogenesis. However, the clinical significance of combined detection of 14-3-3ζ and p-Akt in hepatocellular carcinoma (HCC) remains unclear. Methods: Two-hundred pairs of HCC and adjacent liver specimens were subjected to tissue microarray. The association of 14-3-3ζ and p-Akt levels with the postoperative survival and recurrence in HCC patients was analyzed with univariate and multivariate methods. Moreover, the effects of 14-3-3ζ overexpression on the growth of HCC and the expressions of p-Akt and HIF-1α were assessed in a xenograft mouse model. Results: Elevated levels of 14-3-3ζ and p-Akt were detected in HCC and a positive correlation between the levels of 14-3-3ζ and p-Akt was verified. HCC patients with satellite nodules, microvascular invasion, portal vein tumor thrombosis, poor tumor differentiation and an advanced tumor stage tended to have higher levels of 14-3-3ζ and p-Akt. In addition, the postoperative 3-, 5-, and 7-year overall survival rates in HCC patients with 14-3-3ζ high and p-Akt high were significantly lower compared with those with 14-3-3ζ low and p-Akt low , and the cumulative recurrence rate in HCC patients with 14-3-3ζ high and p-Akt high was significantly higher than that in those with 14-3-3ζ low and p-Akt low . The multivariate Cox proportional hazard analysis indicated that concomitant upregulation of 14-3-3ζ and p-Akt was an independent factor that predicted poor survival and high recurrence in HCC patients. Furthermore, animal experiment showed that overexpression of 14-3-3ζ accelerated the growth of HCC xenograft tumors and induced the expressions of p-Akt and HIF-1α in vivo. Conclusion: Co-upregulation of 14-3-3ζ and p-Akt predicts poor prognosis in patients with HCC, and 14-3-3ζ-induced activation of the Akt signaling pathway contributes to HCC progression.</description><subject>14-3-3 Proteins - genetics</subject><subject>14-3-3 Proteins - metabolism</subject><subject>14-3-3ζ</subject><subject>Aged</subject><subject>Animal research</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - mortality</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Female</subject><subject>Hepatitis</subject><subject>Hepatitis B e Antigens - blood</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Kinases</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>P-Akt</subject><subject>Phosphorylation</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>Surgery</subject><subject>Up-Regulation</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkctu1DAUhiMEoqWwYI9QpG5gEfD9spxGQCtVaoXo2jrjy5BpJg52IsSL8Rg8Ex5SskCsbJ_z-dM5-qvqJUbvMOb6PUKIKUk5flSdYkZwo6VUj8sdYd4oreRJ9SznPSpPqcnT6oRoRjXh_LSKbWzuxuR3cw9TF4c6hhqzhjb0188aBlffNpv7qe5yvck52g4m7-rv3fS1vhls3PnB59I7gp-9nVPyg_VHx6UfYYrW930Rp7qFZLshHuB59SRAn_2Lh_Osuvv44Ut72VzffLpqN9eNZYJODeNCoSCkCBiE4tutBaJI8MFayQWTgSoHpcopc0RQGQQ4C5ptKQ5BCEbPqqvF6yLszZi6A6QfJkJn_hRi2hlIU2d7b2gIVhNNrdecIWu1BRckCY4TxJxVxfVmcY0pfpt9nsyhy8fVYPBxzoYgRAimUumCnv-D7uOchrKpIRhLzJnmpFBvF8qmmHPyYR0QI3NM1KyJFvb1g3HeHrxbyb8RFuDVAtxD2vm0Auv_8_-229uLhTCjC_Q3X0evbw</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Tang, Yufu</creator><creator>Wang, Ruoyu</creator><creator>Zhang, Yibing</creator><creator>Lin, Shenhui</creator><creator>Qiao, Na</creator><creator>Sun, Zhongyi</creator><creator>Cheng, Shuqun</creator><creator>Zhou, Wenping</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>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>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><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Co-Upregulation of 14-3-3ζ and P-Akt is Associated with Oncogenesis and Recurrence of Hepatocellular Carcinoma</title><author>Tang, Yufu ; Wang, Ruoyu ; Zhang, Yibing ; Lin, Shenhui ; Qiao, Na ; Sun, Zhongyi ; Cheng, Shuqun ; Zhou, Wenping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-45680f676f1a685bbca282fefcc75647f38dabbc534d2637f6adca94b31ff6643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>14-3-3 Proteins - genetics</topic><topic>14-3-3 Proteins - metabolism</topic><topic>14-3-3ζ</topic><topic>Aged</topic><topic>Animal research</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - mortality</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Female</topic><topic>Hepatitis</topic><topic>Hepatitis B e Antigens - blood</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Kinases</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>P-Akt</topic><topic>Phosphorylation</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>Surgery</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Yufu</creatorcontrib><creatorcontrib>Wang, Ruoyu</creatorcontrib><creatorcontrib>Zhang, Yibing</creatorcontrib><creatorcontrib>Lin, Shenhui</creatorcontrib><creatorcontrib>Qiao, Na</creatorcontrib><creatorcontrib>Sun, Zhongyi</creatorcontrib><creatorcontrib>Cheng, Shuqun</creatorcontrib><creatorcontrib>Zhou, Wenping</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</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>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>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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Yufu</au><au>Wang, Ruoyu</au><au>Zhang, Yibing</au><au>Lin, Shenhui</au><au>Qiao, Na</au><au>Sun, Zhongyi</au><au>Cheng, Shuqun</au><au>Zhou, Wenping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Co-Upregulation of 14-3-3ζ and P-Akt is Associated with Oncogenesis and Recurrence of Hepatocellular Carcinoma</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>45</volume><issue>3</issue><spage>1097</spage><epage>1107</epage><pages>1097-1107</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: 14-3-3ζ is involved in the regulation of PI3K/Akt pathway which is closely associated with carcinogenesis. However, the clinical significance of combined detection of 14-3-3ζ and p-Akt in hepatocellular carcinoma (HCC) remains unclear. Methods: Two-hundred pairs of HCC and adjacent liver specimens were subjected to tissue microarray. The association of 14-3-3ζ and p-Akt levels with the postoperative survival and recurrence in HCC patients was analyzed with univariate and multivariate methods. Moreover, the effects of 14-3-3ζ overexpression on the growth of HCC and the expressions of p-Akt and HIF-1α were assessed in a xenograft mouse model. Results: Elevated levels of 14-3-3ζ and p-Akt were detected in HCC and a positive correlation between the levels of 14-3-3ζ and p-Akt was verified. HCC patients with satellite nodules, microvascular invasion, portal vein tumor thrombosis, poor tumor differentiation and an advanced tumor stage tended to have higher levels of 14-3-3ζ and p-Akt. In addition, the postoperative 3-, 5-, and 7-year overall survival rates in HCC patients with 14-3-3ζ high and p-Akt high were significantly lower compared with those with 14-3-3ζ low and p-Akt low , and the cumulative recurrence rate in HCC patients with 14-3-3ζ high and p-Akt high was significantly higher than that in those with 14-3-3ζ low and p-Akt low . The multivariate Cox proportional hazard analysis indicated that concomitant upregulation of 14-3-3ζ and p-Akt was an independent factor that predicted poor survival and high recurrence in HCC patients. Furthermore, animal experiment showed that overexpression of 14-3-3ζ accelerated the growth of HCC xenograft tumors and induced the expressions of p-Akt and HIF-1α in vivo. Conclusion: Co-upregulation of 14-3-3ζ and p-Akt predicts poor prognosis in patients with HCC, and 14-3-3ζ-induced activation of the Akt signaling pathway contributes to HCC progression.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29439255</pmid><doi>10.1159/000487351</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 14-3-3 Proteins - genetics 14-3-3 Proteins - metabolism 14-3-3ζ Aged Animal research Animals Apoptosis Cancer therapies Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - mortality Carcinoma, Hepatocellular - pathology Cell cycle Cell Line, Tumor Female Hepatitis Hepatitis B e Antigens - blood Hepatocellular carcinoma Hepatology Humans Hypoxia Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Kinases Liver - metabolism Liver - pathology Liver cancer Liver Neoplasms - metabolism Liver Neoplasms - pathology Male Medical prognosis Metastasis Mice Mice, Inbred BALB C Mice, Nude Middle Aged Original Paper P-Akt Phosphorylation Prognosis Proteins Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Surgery Up-Regulation |
| title | Co-Upregulation of 14-3-3ζ and P-Akt is Associated with Oncogenesis and Recurrence of Hepatocellular Carcinoma |
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