Gankyrin promotes breast cancer cell metastasis by regulating Rac1 activity
Tumor metastasis is responsible for most cancer patients’ deaths. Understanding the mechanism of metastasis is crucial for improving the cure rate for cancer. Here, we report that Gankyrin, a chaperone of ubiquitin–proteasome, has an essential role in breast cancer metastasis. We find that Gankyrin...
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| Veröffentlicht in: | Oncogene 2013-07, Vol.32 (29), p.3452-3460 |
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| creator | Zhen, C Chen, L Zhao, Q Liang, B Gu, Y-X Bai, Z-f Wang, K Xu, X Han, Q-y Fang, D-f Wang, S-x Zhou, T Xia, Q Gong, W-l Wang, N Li, H-Y Jin, B-F Man, J-h |
| description | Tumor metastasis is responsible for most cancer patients’ deaths. Understanding the mechanism of metastasis is crucial for improving the cure rate for cancer. Here, we report that Gankyrin, a chaperone of ubiquitin–proteasome, has an essential role in breast cancer metastasis. We find that Gankyrin is highly overexpressed in human breast cancers and the expression correlates strongly with lymph node metastasis. Knocking down Gankyrin expression in highly metastatic human breast cancer cells significantly decreases cancer cell migration and invasion. Furthermore, we demonstrate that depletion of Gankyrin inhibits intrinsic Rac1 activity and induces large focal adhesions. Overexpression of Gankyrin accelerates focal adhesion turnover and increases cell migration. Notably, reduction of Gankyrin expression in mouse mammary tumor cell significantly decreases tumor metastasis to lung in animal models. Therefore, our findings suggest that Gankyrin is crucial for breast cancer metastasis and highlight the potential of Gankyrin as a therapeutic target for tumor metastasis. |
| doi_str_mv | 10.1038/onc.2012.356 |
| format | Article |
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Understanding the mechanism of metastasis is crucial for improving the cure rate for cancer. Here, we report that Gankyrin, a chaperone of ubiquitin–proteasome, has an essential role in breast cancer metastasis. We find that Gankyrin is highly overexpressed in human breast cancers and the expression correlates strongly with lymph node metastasis. Knocking down Gankyrin expression in highly metastatic human breast cancer cells significantly decreases cancer cell migration and invasion. Furthermore, we demonstrate that depletion of Gankyrin inhibits intrinsic Rac1 activity and induces large focal adhesions. Overexpression of Gankyrin accelerates focal adhesion turnover and increases cell migration. Notably, reduction of Gankyrin expression in mouse mammary tumor cell significantly decreases tumor metastasis to lung in animal models. Therefore, our findings suggest that Gankyrin is crucial for breast cancer metastasis and highlight the potential of Gankyrin as a therapeutic target for tumor metastasis.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2012.356</identifier><identifier>PMID: 22890318</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/45/612/1243 ; 692/699/67/1347 ; 692/699/67/322 ; Animal models ; Animals ; Apoptosis ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell adhesion & migration ; Cell Biology ; Cell Line ; Cell migration ; Development and progression ; Disease Models, Animal ; Gene expression ; Gene Knockdown Techniques ; Genetic aspects ; Human Genetics ; Humans ; Immunohistochemistry ; Internal Medicine ; Lymph nodes ; Mammary gland ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; Mice ; Mice, Inbred BALB C ; Neoplasm Invasiveness - pathology ; Oncology ; original-article ; Physiological aspects ; Proteasome Endopeptidase Complex - metabolism ; Proteasomes ; Proto-Oncogene Proteins - metabolism ; rac1 GTP-Binding Protein - metabolism ; Rac1 protein ; Risk factors ; RNA, Small Interfering ; Signal Transduction - physiology ; Therapeutic targets ; Transfection ; Tumors ; Ubiquitin ; Ubiquitin-proteasome system</subject><ispartof>Oncogene, 2013-07, Vol.32 (29), p.3452-3460</ispartof><rights>Macmillan Publishers Limited 2013</rights><rights>COPYRIGHT 2013 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 18, 2013</rights><rights>Macmillan Publishers Limited 2013.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c523t-e72ce1b461165a7c35fbc3f22d613cc0c0f6a24c53cc4fa13fe8dfe60a6e9bc43</citedby><cites>FETCH-LOGICAL-c523t-e72ce1b461165a7c35fbc3f22d613cc0c0f6a24c53cc4fa13fe8dfe60a6e9bc43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2012.356$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2012.356$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22890318$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhen, C</creatorcontrib><creatorcontrib>Chen, L</creatorcontrib><creatorcontrib>Zhao, Q</creatorcontrib><creatorcontrib>Liang, B</creatorcontrib><creatorcontrib>Gu, Y-X</creatorcontrib><creatorcontrib>Bai, Z-f</creatorcontrib><creatorcontrib>Wang, K</creatorcontrib><creatorcontrib>Xu, X</creatorcontrib><creatorcontrib>Han, Q-y</creatorcontrib><creatorcontrib>Fang, D-f</creatorcontrib><creatorcontrib>Wang, S-x</creatorcontrib><creatorcontrib>Zhou, T</creatorcontrib><creatorcontrib>Xia, Q</creatorcontrib><creatorcontrib>Gong, W-l</creatorcontrib><creatorcontrib>Wang, N</creatorcontrib><creatorcontrib>Li, H-Y</creatorcontrib><creatorcontrib>Jin, B-F</creatorcontrib><creatorcontrib>Man, J-h</creatorcontrib><title>Gankyrin promotes breast cancer cell metastasis by regulating Rac1 activity</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Tumor metastasis is responsible for most cancer patients’ deaths. Understanding the mechanism of metastasis is crucial for improving the cure rate for cancer. Here, we report that Gankyrin, a chaperone of ubiquitin–proteasome, has an essential role in breast cancer metastasis. We find that Gankyrin is highly overexpressed in human breast cancers and the expression correlates strongly with lymph node metastasis. Knocking down Gankyrin expression in highly metastatic human breast cancer cells significantly decreases cancer cell migration and invasion. Furthermore, we demonstrate that depletion of Gankyrin inhibits intrinsic Rac1 activity and induces large focal adhesions. Overexpression of Gankyrin accelerates focal adhesion turnover and increases cell migration. Notably, reduction of Gankyrin expression in mouse mammary tumor cell significantly decreases tumor metastasis to lung in animal models. Therefore, our findings suggest that Gankyrin is crucial for breast cancer metastasis and highlight the potential of Gankyrin as a therapeutic target for tumor metastasis.</description><subject>631/45/612/1243</subject><subject>692/699/67/1347</subject><subject>692/699/67/322</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Cell migration</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>Genetic aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Internal Medicine</subject><subject>Lymph nodes</subject><subject>Mammary gland</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Neoplasm Invasiveness - 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Understanding the mechanism of metastasis is crucial for improving the cure rate for cancer. Here, we report that Gankyrin, a chaperone of ubiquitin–proteasome, has an essential role in breast cancer metastasis. We find that Gankyrin is highly overexpressed in human breast cancers and the expression correlates strongly with lymph node metastasis. Knocking down Gankyrin expression in highly metastatic human breast cancer cells significantly decreases cancer cell migration and invasion. Furthermore, we demonstrate that depletion of Gankyrin inhibits intrinsic Rac1 activity and induces large focal adhesions. Overexpression of Gankyrin accelerates focal adhesion turnover and increases cell migration. Notably, reduction of Gankyrin expression in mouse mammary tumor cell significantly decreases tumor metastasis to lung in animal models. 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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | 631/45/612/1243 692/699/67/1347 692/699/67/322 Animal models Animals Apoptosis Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell adhesion & migration Cell Biology Cell Line Cell migration Development and progression Disease Models, Animal Gene expression Gene Knockdown Techniques Genetic aspects Human Genetics Humans Immunohistochemistry Internal Medicine Lymph nodes Mammary gland Medicine Medicine & Public Health Metastases Metastasis Mice Mice, Inbred BALB C Neoplasm Invasiveness - pathology Oncology original-article Physiological aspects Proteasome Endopeptidase Complex - metabolism Proteasomes Proto-Oncogene Proteins - metabolism rac1 GTP-Binding Protein - metabolism Rac1 protein Risk factors RNA, Small Interfering Signal Transduction - physiology Therapeutic targets Transfection Tumors Ubiquitin Ubiquitin-proteasome system |
| title | Gankyrin promotes breast cancer cell metastasis by regulating Rac1 activity |
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