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The overexpression of Rab9 promotes tumor progression regulated by XBP1 in breast cancer
Rab9 is a small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes and is involved in the recycling of mannose-6-phosphate receptors (MPRs). To determine new treatment strategies for breast cancer and to elucidate the mechanism underlying the phenomenon, we investigated the ef...
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Published in: | OncoTargets and therapy 2019-01, Vol.12, p.1815-1824 |
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creator | Liu, Yansong Wang, Xin Zhang, Zhonghua Xiao, Bin An, Baoming Zhang, Jun |
description | Rab9 is a small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes and is involved in the recycling of mannose-6-phosphate receptors (MPRs).
To determine new treatment strategies for breast cancer and to elucidate the mechanism underlying the phenomenon, we investigated the effects of Rab9 in the human breast cancer cell lines MCF7 and MDA-MB-231.
We observed that knockdown of Rab9 inhibited the survival and proliferation of MCF7 and MDA-MB-231 cells, whereas Rab9 overexpression facilitated cell survival and proliferation by inducing or suppressing apoptosis. These results were further confirmed by the Bax/Bcl-2 ratio in affected MCF7 and MDA-MB-231 cells, which demonstrated whether the mitochondrial apoptotic pathway was triggered. Furthermore, the AKT/PI3K pathway is implicated in cell growth and survival and Rab9 changed the expression and phosphorylation of PI3K signaling pathway members. XBP1 is a key regulator of Rab9 and further confirmed that Rab9 play important roles in breast cancer tumorigenesis.
These data suggest that Rab9 is a good candidate for a novel therapeutic strategy for the treatment of breast cancer. |
doi_str_mv | 10.2147/OTT.S183748 |
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To determine new treatment strategies for breast cancer and to elucidate the mechanism underlying the phenomenon, we investigated the effects of Rab9 in the human breast cancer cell lines MCF7 and MDA-MB-231.
We observed that knockdown of Rab9 inhibited the survival and proliferation of MCF7 and MDA-MB-231 cells, whereas Rab9 overexpression facilitated cell survival and proliferation by inducing or suppressing apoptosis. These results were further confirmed by the Bax/Bcl-2 ratio in affected MCF7 and MDA-MB-231 cells, which demonstrated whether the mitochondrial apoptotic pathway was triggered. Furthermore, the AKT/PI3K pathway is implicated in cell growth and survival and Rab9 changed the expression and phosphorylation of PI3K signaling pathway members. XBP1 is a key regulator of Rab9 and further confirmed that Rab9 play important roles in breast cancer tumorigenesis.
These data suggest that Rab9 is a good candidate for a novel therapeutic strategy for the treatment of breast cancer.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S183748</identifier><identifier>PMID: 30881034</identifier><language>eng</language><publisher>New Zealand: Taylor & Francis Ltd</publisher><subject>Antibiotics ; Apoptosis ; Breast cancer ; Cell adhesion & migration ; Cell growth ; Experiments ; Immunoglobulins ; Kinases ; Metastasis ; Mitochondria ; Original Research ; Plasmids ; Proteins</subject><ispartof>OncoTargets and therapy, 2019-01, Vol.12, p.1815-1824</ispartof><rights>2019. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Liu et al. This work is published and licensed by Dove Medical Press Limited 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-bff0146bed6eeca0fdc5b00907492df6af0e4d03972059cc6fdccf78337264793</citedby><orcidid>0000-0002-0748-3143</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2229634897/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2229634897?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30881034$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yansong</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Zhang, Zhonghua</creatorcontrib><creatorcontrib>Xiao, Bin</creatorcontrib><creatorcontrib>An, Baoming</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><title>The overexpression of Rab9 promotes tumor progression regulated by XBP1 in breast cancer</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>Rab9 is a small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes and is involved in the recycling of mannose-6-phosphate receptors (MPRs).
To determine new treatment strategies for breast cancer and to elucidate the mechanism underlying the phenomenon, we investigated the effects of Rab9 in the human breast cancer cell lines MCF7 and MDA-MB-231.
We observed that knockdown of Rab9 inhibited the survival and proliferation of MCF7 and MDA-MB-231 cells, whereas Rab9 overexpression facilitated cell survival and proliferation by inducing or suppressing apoptosis. These results were further confirmed by the Bax/Bcl-2 ratio in affected MCF7 and MDA-MB-231 cells, which demonstrated whether the mitochondrial apoptotic pathway was triggered. Furthermore, the AKT/PI3K pathway is implicated in cell growth and survival and Rab9 changed the expression and phosphorylation of PI3K signaling pathway members. XBP1 is a key regulator of Rab9 and further confirmed that Rab9 play important roles in breast cancer tumorigenesis.
These data suggest that Rab9 is a good candidate for a novel therapeutic strategy for the treatment of breast cancer.</description><subject>Antibiotics</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Experiments</subject><subject>Immunoglobulins</subject><subject>Kinases</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>Original Research</subject><subject>Plasmids</subject><subject>Proteins</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkctLAzEQxoMoWh8n7xLwIkg1ryabi6DiCwRFK_QWstlJ3bK7qcmu6H_vFmtRTzPD_PjmGz6E9ik5YVSo04fx-OSZZlyJbA0NKFXZUGpO1n_1W2g7pRkhUmZMbKItTrKMEi4GaDJ-BRzeIcLHPEJKZWhw8PjJ5hrPY6hDCwm3XR3iYpz-IBGmXWVbKHD-iScXjxSXDc4j2NRiZxsHcRdteFsl2FvWHfRyfTW-vB3eP9zcXZ7fD50Y0XaYe0-okDkUEsBZ4gs3ygnRRAnNCi-tJyAKwrViZKSdkz3gvMo4V0wKpfkOOvvWnXd5DYWDpo22MvNY1jZ-mmBL83fTlK9mGt6NFERIpXqBo6VADG8dpNbUZXJQVbaB0CXDqOaS9tdGPXr4D52FLjb9e4YxpiUXmV4IHn9TLoaUIviVGUrMIjHTJ2aWifX0wW__K_YnIv4FnJKScg</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Liu, Yansong</creator><creator>Wang, Xin</creator><creator>Zhang, Zhonghua</creator><creator>Xiao, Bin</creator><creator>An, Baoming</creator><creator>Zhang, Jun</creator><general>Taylor & Francis Ltd</general><general>Dove Medical Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</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><orcidid>https://orcid.org/0000-0002-0748-3143</orcidid></search><sort><creationdate>20190101</creationdate><title>The overexpression of Rab9 promotes tumor progression regulated by XBP1 in breast cancer</title><author>Liu, Yansong ; Wang, Xin ; Zhang, Zhonghua ; Xiao, Bin ; An, Baoming ; Zhang, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-bff0146bed6eeca0fdc5b00907492df6af0e4d03972059cc6fdccf78337264793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antibiotics</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Experiments</topic><topic>Immunoglobulins</topic><topic>Kinases</topic><topic>Metastasis</topic><topic>Mitochondria</topic><topic>Original Research</topic><topic>Plasmids</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yansong</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Zhang, Zhonghua</creatorcontrib><creatorcontrib>Xiao, Bin</creatorcontrib><creatorcontrib>An, Baoming</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest research library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yansong</au><au>Wang, Xin</au><au>Zhang, Zhonghua</au><au>Xiao, Bin</au><au>An, Baoming</au><au>Zhang, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The overexpression of Rab9 promotes tumor progression regulated by XBP1 in breast cancer</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>12</volume><spage>1815</spage><epage>1824</epage><pages>1815-1824</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>Rab9 is a small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes and is involved in the recycling of mannose-6-phosphate receptors (MPRs).
To determine new treatment strategies for breast cancer and to elucidate the mechanism underlying the phenomenon, we investigated the effects of Rab9 in the human breast cancer cell lines MCF7 and MDA-MB-231.
We observed that knockdown of Rab9 inhibited the survival and proliferation of MCF7 and MDA-MB-231 cells, whereas Rab9 overexpression facilitated cell survival and proliferation by inducing or suppressing apoptosis. These results were further confirmed by the Bax/Bcl-2 ratio in affected MCF7 and MDA-MB-231 cells, which demonstrated whether the mitochondrial apoptotic pathway was triggered. Furthermore, the AKT/PI3K pathway is implicated in cell growth and survival and Rab9 changed the expression and phosphorylation of PI3K signaling pathway members. XBP1 is a key regulator of Rab9 and further confirmed that Rab9 play important roles in breast cancer tumorigenesis.
These data suggest that Rab9 is a good candidate for a novel therapeutic strategy for the treatment of breast cancer.</abstract><cop>New Zealand</cop><pub>Taylor & Francis Ltd</pub><pmid>30881034</pmid><doi>10.2147/OTT.S183748</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-0748-3143</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibiotics Apoptosis Breast cancer Cell adhesion & migration Cell growth Experiments Immunoglobulins Kinases Metastasis Mitochondria Original Research Plasmids Proteins |
title | The overexpression of Rab9 promotes tumor progression regulated by XBP1 in breast cancer |
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