Downregulation of hepatoma-derived growth factor activates the Bad-mediated apoptotic pathway in human cancer cells
Hepatoma-derived growth factor (HDGF) is highly expressed in human cancer and its expression is correlated with poor prognosis of cancer. The growth factor is known to stimulate cell growth while the underlying mechanism is however not clear. Transfection with HDGF cDNA stimulated while its specific...
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| Veröffentlicht in: | Apoptosis (London) 2008-09, Vol.13 (9), p.1135-1147 |
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| creator | Tsang, Tsun Yee Tang, Wan Yee Tsang, Wing Pui Co, Ngai Na Kong, Siu Kai Kwok, Tim Tak |
| description | Hepatoma-derived growth factor (HDGF) is highly expressed in human cancer and its expression is correlated with poor prognosis of cancer. The growth factor is known to stimulate cell growth while the underlying mechanism is however not clear. Transfection with HDGF cDNA stimulated while its specific antisense oligonucleotides repressed the growth of human hepatocellular carcinoma HepG2 cells. Furthermore, knock-down of HDGF by antisense oligos also induced apoptosis in HepG2 cells and in other human cancer cells, e.g. human squamous carcinoma A431 cells. HDGF knock-down was found to induce the expression of the pro-apoptotic protein Bad and also inactivate ERK and Akt, which in turn led to dephosphorylation of Bad at Ser-112, Ser-136, and activation of the intrinsic apoptotic pathway, i.e. depolarization of the mitochondrial membrane, release of mitochondrial cytochrome c, increase in the processing of caspase 9 and 3. As HDGF knock-down not only suppresses the growth but also induces apoptosis in human cancer cells, HDGF may therefore serve as a survival factor for human cancer cells and a potential target for cancer therapy. |
| doi_str_mv | 10.1007/s10495-008-0241-6 |
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The growth factor is known to stimulate cell growth while the underlying mechanism is however not clear. Transfection with HDGF cDNA stimulated while its specific antisense oligonucleotides repressed the growth of human hepatocellular carcinoma HepG2 cells. Furthermore, knock-down of HDGF by antisense oligos also induced apoptosis in HepG2 cells and in other human cancer cells, e.g. human squamous carcinoma A431 cells. HDGF knock-down was found to induce the expression of the pro-apoptotic protein Bad and also inactivate ERK and Akt, which in turn led to dephosphorylation of Bad at Ser-112, Ser-136, and activation of the intrinsic apoptotic pathway, i.e. depolarization of the mitochondrial membrane, release of mitochondrial cytochrome c, increase in the processing of caspase 9 and 3. As HDGF knock-down not only suppresses the growth but also induces apoptosis in human cancer cells, HDGF may therefore serve as a survival factor for human cancer cells and a potential target for cancer therapy.</description><identifier>ISSN: 1360-8185</identifier><identifier>EISSN: 1573-675X</identifier><identifier>DOI: 10.1007/s10495-008-0241-6</identifier><identifier>PMID: 18651222</identifier><language>eng</language><publisher>Boston: Boston : Springer US</publisher><subject>Apoptosis ; bcl-Associated Death Protein - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Colforsin - pharmacology ; Down-Regulation - drug effects ; Epidermal Growth Factor - pharmacology ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Intercellular Signaling Peptides and Proteins - genetics ; Neoplasms - enzymology ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Oncology ; Original Paper ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Virology</subject><ispartof>Apoptosis (London), 2008-09, Vol.13 (9), p.1135-1147</ispartof><rights>Springer Science+Business Media, LLC 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-14f5ff092ef7816dac1d9fa3826f8d823c4580384824215569e92d119d1f1bb43</citedby><cites>FETCH-LOGICAL-c459t-14f5ff092ef7816dac1d9fa3826f8d823c4580384824215569e92d119d1f1bb43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10495-008-0241-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10495-008-0241-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18651222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsang, Tsun Yee</creatorcontrib><creatorcontrib>Tang, Wan Yee</creatorcontrib><creatorcontrib>Tsang, Wing Pui</creatorcontrib><creatorcontrib>Co, Ngai Na</creatorcontrib><creatorcontrib>Kong, Siu Kai</creatorcontrib><creatorcontrib>Kwok, Tim Tak</creatorcontrib><title>Downregulation of hepatoma-derived growth factor activates the Bad-mediated apoptotic pathway in human cancer cells</title><title>Apoptosis (London)</title><addtitle>Apoptosis</addtitle><addtitle>Apoptosis</addtitle><description>Hepatoma-derived growth factor (HDGF) is highly expressed in human cancer and its expression is correlated with poor prognosis of cancer. The growth factor is known to stimulate cell growth while the underlying mechanism is however not clear. Transfection with HDGF cDNA stimulated while its specific antisense oligonucleotides repressed the growth of human hepatocellular carcinoma HepG2 cells. Furthermore, knock-down of HDGF by antisense oligos also induced apoptosis in HepG2 cells and in other human cancer cells, e.g. human squamous carcinoma A431 cells. HDGF knock-down was found to induce the expression of the pro-apoptotic protein Bad and also inactivate ERK and Akt, which in turn led to dephosphorylation of Bad at Ser-112, Ser-136, and activation of the intrinsic apoptotic pathway, i.e. depolarization of the mitochondrial membrane, release of mitochondrial cytochrome c, increase in the processing of caspase 9 and 3. As HDGF knock-down not only suppresses the growth but also induces apoptosis in human cancer cells, HDGF may therefore serve as a survival factor for human cancer cells and a potential target for cancer therapy.</description><subject>Apoptosis</subject><subject>bcl-Associated Death Protein - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Colforsin - pharmacology</subject><subject>Down-Regulation - drug effects</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Neoplasms - enzymology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Virology</subject><issn>1360-8185</issn><issn>1573-675X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUtv3CAUha2qVfNofkA3LeoiO5p7wWC8bNOnFCmLNlJ2iDEwdjQ2LuCM8u_LyCNF6qIbQPDdcy_nVNVbhI8I0FwlhLoVFEBRYDVS-aI6RdFwKhtx_7KcuQSqUImT6iylBwDgitevqxNUUiBj7LRKX8J-im677EwewkSCJ72bTQ6jodbF4dFZso1hn3viTZdDJGUdHk12ieTekc_G0tHZoVxYYuYw55CHjhSFfm-eyDCRfhnNRDozdS6Szu126U31yptdchfH_by6-_b19_UPenP7_ef1pxva1aLNFGsvvIeWOd8olNZ0aFtvuGLSK6sYL5gqP6oVqxkKIVvXMovYWvS42dT8vLpcdecY_iwuZT0O6TCBmVxYkpZtDQ1veAE__AM-hCVOZTbNioUtcDio4Qp1MaQUnddzHEYTnzSCPsSh1zh0iUMf4tCy1Lw7Ci-b4tJzxdH_ArAVSOVp2rr43Pl_qu_XIm-CNts4JH33iwFyKGZJBoL_BXp6nvk</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Tsang, Tsun Yee</creator><creator>Tang, Wan Yee</creator><creator>Tsang, Wing Pui</creator><creator>Co, Ngai Na</creator><creator>Kong, Siu Kai</creator><creator>Kwok, Tim Tak</creator><general>Boston : Springer US</general><general>Springer US</general><general>Springer Nature B.V</general><scope>FBQ</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>7QL</scope><scope>7QP</scope><scope>7RQ</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20080901</creationdate><title>Downregulation of hepatoma-derived growth factor activates the Bad-mediated apoptotic pathway in human cancer cells</title><author>Tsang, Tsun Yee ; Tang, Wan Yee ; Tsang, Wing Pui ; Co, Ngai Na ; Kong, Siu Kai ; Kwok, Tim Tak</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-14f5ff092ef7816dac1d9fa3826f8d823c4580384824215569e92d119d1f1bb43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Apoptosis</topic><topic>bcl-Associated Death Protein - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Colforsin - pharmacology</topic><topic>Down-Regulation - drug effects</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Neoplasms - enzymology</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsang, Tsun Yee</creatorcontrib><creatorcontrib>Tang, Wan Yee</creatorcontrib><creatorcontrib>Tsang, Wing Pui</creatorcontrib><creatorcontrib>Co, Ngai Na</creatorcontrib><creatorcontrib>Kong, Siu Kai</creatorcontrib><creatorcontrib>Kwok, Tim Tak</creatorcontrib><collection>AGRIS</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</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>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science 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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Apoptosis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsang, Tsun Yee</au><au>Tang, Wan Yee</au><au>Tsang, Wing Pui</au><au>Co, Ngai Na</au><au>Kong, Siu Kai</au><au>Kwok, Tim Tak</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulation of hepatoma-derived growth factor activates the Bad-mediated apoptotic pathway in human cancer cells</atitle><jtitle>Apoptosis (London)</jtitle><stitle>Apoptosis</stitle><addtitle>Apoptosis</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>13</volume><issue>9</issue><spage>1135</spage><epage>1147</epage><pages>1135-1147</pages><issn>1360-8185</issn><eissn>1573-675X</eissn><abstract>Hepatoma-derived growth factor (HDGF) is highly expressed in human cancer and its expression is correlated with poor prognosis of cancer. The growth factor is known to stimulate cell growth while the underlying mechanism is however not clear. Transfection with HDGF cDNA stimulated while its specific antisense oligonucleotides repressed the growth of human hepatocellular carcinoma HepG2 cells. Furthermore, knock-down of HDGF by antisense oligos also induced apoptosis in HepG2 cells and in other human cancer cells, e.g. human squamous carcinoma A431 cells. HDGF knock-down was found to induce the expression of the pro-apoptotic protein Bad and also inactivate ERK and Akt, which in turn led to dephosphorylation of Bad at Ser-112, Ser-136, and activation of the intrinsic apoptotic pathway, i.e. depolarization of the mitochondrial membrane, release of mitochondrial cytochrome c, increase in the processing of caspase 9 and 3. As HDGF knock-down not only suppresses the growth but also induces apoptosis in human cancer cells, HDGF may therefore serve as a survival factor for human cancer cells and a potential target for cancer therapy.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>18651222</pmid><doi>10.1007/s10495-008-0241-6</doi><tpages>13</tpages></addata></record> |
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| subjects | Apoptosis bcl-Associated Death Protein - metabolism Biochemistry Biomedical and Life Sciences Biomedicine Cancer Research Cell Biology Cell Line, Tumor Cell Proliferation - drug effects Colforsin - pharmacology Down-Regulation - drug effects Epidermal Growth Factor - pharmacology Extracellular Signal-Regulated MAP Kinases - metabolism Gene Expression Regulation, Neoplastic - drug effects Humans Intercellular Signaling Peptides and Proteins - genetics Neoplasms - enzymology Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Oncology Original Paper Phosphorylation - drug effects Proto-Oncogene Proteins c-akt - metabolism Virology |
| title | Downregulation of hepatoma-derived growth factor activates the Bad-mediated apoptotic pathway in human cancer cells |
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