MiR‐142‐3p functions as a tumor suppressor by targeting RAC1/PAK1 pathway in breast cancer
MicroRNA‐142‐3p (miR‐142‐3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR‐142‐3p was markedly decreased both in cell lines and BC tumor tissues. Elevated miR‐142‐3p expression suppressed gr...
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| Veröffentlicht in: | Journal of cellular physiology 2020-05, Vol.235 (5), p.4928-4940 |
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| creator | Xu, Tao He, Bang‐Shun Pan, Bei Pan, Yu‐Qin Sun, Hui‐Ling Liu, Xiang‐Xiang Xu, Xue‐Ni Chen, Xiao‐Xiang Zeng, Kai‐Xuan Xu, Mu Wang, Shu‐Kui |
| description | MicroRNA‐142‐3p (miR‐142‐3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR‐142‐3p was markedly decreased both in cell lines and BC tumor tissues. Elevated miR‐142‐3p expression suppressed growth and metastasis of BC cell lines via gain‐of‐function assay in vitro and in vivo. Mechanistically, miR‐142‐3p could regulate the ras‐related C3 botulinum toxin substrate 1 (RAC1) expression in protein level, which simultaneously suppressed the epithelial‐to‐mesenchymal transition related protein levels and the activity of PAK1 phosphorylation, respectively. In addition, rescue experiments revealed RAC1 overexpression could reverse tumor‐suppressive role of miR‐142‐3p. Our results showed miR‐142‐3p could function as a tumor suppressor via targeting RAC1/PAK1 pathway in BC, suggesting a potent therapeutic target for BC treatment.
MiR‐142‐3p is downregulated in breast cancer (BC) tissues and cell lines. MiR‐142‐3p may act as a tumor suppressor by regulating cell proliferation, migration, invasion, angiogenesis, and epithelial‐to‐mesenchymal transition process through directly downregulation of ras‐related C3 botulinum toxin substrate 1 expression and subsequently inhibiting the activity of PAK1 phosphorylation in BC. |
| doi_str_mv | 10.1002/jcp.29372 |
| format | Article |
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MiR‐142‐3p is downregulated in breast cancer (BC) tissues and cell lines. MiR‐142‐3p may act as a tumor suppressor by regulating cell proliferation, migration, invasion, angiogenesis, and epithelial‐to‐mesenchymal transition process through directly downregulation of ras‐related C3 botulinum toxin substrate 1 expression and subsequently inhibiting the activity of PAK1 phosphorylation in BC.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.29372</identifier><identifier>PMID: 31674013</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; Biotechnology ; Botulinum toxin ; Breast cancer ; Breast Neoplasms - enzymology ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cell Movement ; Cell Proliferation ; Databases, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MCF-7 Cells ; Mesenchyme ; Metastases ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; miR‐142‐3p ; Neoplasm Invasiveness ; Neovascularization, Pathologic ; p21-Activated Kinases - genetics ; p21-Activated Kinases - metabolism ; PAK1 ; Phosphorylation ; Proteins ; RAC1 ; rac1 GTP-Binding Protein - genetics ; rac1 GTP-Binding Protein - metabolism ; Rac1 protein ; Signal Transduction ; Substrates ; Therapeutic applications ; Toxins ; Tumor cell lines ; Tumor suppressor genes ; Tumors</subject><ispartof>Journal of cellular physiology, 2020-05, Vol.235 (5), p.4928-4940</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-310c6a3442fb9f3d7e6d3293f71674c487dfd3f01aa4e9d970c86f2d567764d53</citedby><cites>FETCH-LOGICAL-c3532-310c6a3442fb9f3d7e6d3293f71674c487dfd3f01aa4e9d970c86f2d567764d53</cites><orcidid>0000-0001-6972-2587</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.29372$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.29372$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31674013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Tao</creatorcontrib><creatorcontrib>He, Bang‐Shun</creatorcontrib><creatorcontrib>Pan, Bei</creatorcontrib><creatorcontrib>Pan, Yu‐Qin</creatorcontrib><creatorcontrib>Sun, Hui‐Ling</creatorcontrib><creatorcontrib>Liu, Xiang‐Xiang</creatorcontrib><creatorcontrib>Xu, Xue‐Ni</creatorcontrib><creatorcontrib>Chen, Xiao‐Xiang</creatorcontrib><creatorcontrib>Zeng, Kai‐Xuan</creatorcontrib><creatorcontrib>Xu, Mu</creatorcontrib><creatorcontrib>Wang, Shu‐Kui</creatorcontrib><title>MiR‐142‐3p functions as a tumor suppressor by targeting RAC1/PAK1 pathway in breast cancer</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>MicroRNA‐142‐3p (miR‐142‐3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR‐142‐3p was markedly decreased both in cell lines and BC tumor tissues. Elevated miR‐142‐3p expression suppressed growth and metastasis of BC cell lines via gain‐of‐function assay in vitro and in vivo. Mechanistically, miR‐142‐3p could regulate the ras‐related C3 botulinum toxin substrate 1 (RAC1) expression in protein level, which simultaneously suppressed the epithelial‐to‐mesenchymal transition related protein levels and the activity of PAK1 phosphorylation, respectively. In addition, rescue experiments revealed RAC1 overexpression could reverse tumor‐suppressive role of miR‐142‐3p. Our results showed miR‐142‐3p could function as a tumor suppressor via targeting RAC1/PAK1 pathway in BC, suggesting a potent therapeutic target for BC treatment.
MiR‐142‐3p is downregulated in breast cancer (BC) tissues and cell lines. MiR‐142‐3p may act as a tumor suppressor by regulating cell proliferation, migration, invasion, angiogenesis, and epithelial‐to‐mesenchymal transition process through directly downregulation of ras‐related C3 botulinum toxin substrate 1 expression and subsequently inhibiting the activity of PAK1 phosphorylation in BC.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Botulinum toxin</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Databases, Genetic</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>MCF-7 Cells</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>miR‐142‐3p</subject><subject>Neoplasm Invasiveness</subject><subject>Neovascularization, Pathologic</subject><subject>p21-Activated Kinases - genetics</subject><subject>p21-Activated Kinases - metabolism</subject><subject>PAK1</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>RAC1</subject><subject>rac1 GTP-Binding Protein - genetics</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>Rac1 protein</subject><subject>Signal Transduction</subject><subject>Substrates</subject><subject>Therapeutic applications</subject><subject>Toxins</subject><subject>Tumor cell lines</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kN1KwzAYhoMobk4PvAEJeKIH3fLXpjkcw3_FMfTUkqbJ7OjamrSMnXkJXqNXYmanB4IQkg--h4c3LwDHGA0xQmS0UPWQCMrJDuhjJHjAopDsgr7f4UCEDPfAgXMLhJAQlO6DHsURZwjTPnh5yGef7x-YEX_TGpq2VE1elQ5Kf2DTLisLXVvXVjvnx3QNG2nnusnLOZyNJ3g0Hd9hWMvmdSXXMC9harV0DVSyVNoegj0jC6ePtu8APF9ePE2ug_vHq5vJ-D5QNKQkoBipSFLGiEmFoRnXUUb9jwzfBFUs5pnJqEFYSqZFJjhScWRIFkacRywL6QCcdd7aVm-tdk2yzJ3SRSFLXbUuIRTjKOQIxR49_YMuqtaWPp2nQsoEI_FGeN5RylbOWW2S2uZLadcJRsmm9MSXnnyX7tmTrbFNlzr7JX9a9sCoA1Z5odf_m5LbybRTfgHv6oo6</recordid><startdate>202005</startdate><enddate>202005</enddate><creator>Xu, Tao</creator><creator>He, Bang‐Shun</creator><creator>Pan, Bei</creator><creator>Pan, Yu‐Qin</creator><creator>Sun, Hui‐Ling</creator><creator>Liu, Xiang‐Xiang</creator><creator>Xu, Xue‐Ni</creator><creator>Chen, Xiao‐Xiang</creator><creator>Zeng, Kai‐Xuan</creator><creator>Xu, Mu</creator><creator>Wang, Shu‐Kui</creator><general>Wiley Subscription Services, Inc</general><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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6972-2587</orcidid></search><sort><creationdate>202005</creationdate><title>MiR‐142‐3p functions as a tumor suppressor by targeting RAC1/PAK1 pathway in breast cancer</title><author>Xu, Tao ; He, Bang‐Shun ; Pan, Bei ; Pan, Yu‐Qin ; Sun, Hui‐Ling ; Liu, Xiang‐Xiang ; Xu, Xue‐Ni ; Chen, Xiao‐Xiang ; Zeng, Kai‐Xuan ; Xu, Mu ; Wang, Shu‐Kui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-310c6a3442fb9f3d7e6d3293f71674c487dfd3f01aa4e9d970c86f2d567764d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biotechnology</topic><topic>Botulinum toxin</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Databases, Genetic</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>MCF-7 Cells</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>miR‐142‐3p</topic><topic>Neoplasm Invasiveness</topic><topic>Neovascularization, Pathologic</topic><topic>p21-Activated Kinases - genetics</topic><topic>p21-Activated Kinases - metabolism</topic><topic>PAK1</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>RAC1</topic><topic>rac1 GTP-Binding Protein - genetics</topic><topic>rac1 GTP-Binding Protein - metabolism</topic><topic>Rac1 protein</topic><topic>Signal Transduction</topic><topic>Substrates</topic><topic>Therapeutic applications</topic><topic>Toxins</topic><topic>Tumor cell lines</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Tao</creatorcontrib><creatorcontrib>He, Bang‐Shun</creatorcontrib><creatorcontrib>Pan, Bei</creatorcontrib><creatorcontrib>Pan, Yu‐Qin</creatorcontrib><creatorcontrib>Sun, Hui‐Ling</creatorcontrib><creatorcontrib>Liu, Xiang‐Xiang</creatorcontrib><creatorcontrib>Xu, Xue‐Ni</creatorcontrib><creatorcontrib>Chen, Xiao‐Xiang</creatorcontrib><creatorcontrib>Zeng, Kai‐Xuan</creatorcontrib><creatorcontrib>Xu, Mu</creatorcontrib><creatorcontrib>Wang, Shu‐Kui</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Tao</au><au>He, Bang‐Shun</au><au>Pan, Bei</au><au>Pan, Yu‐Qin</au><au>Sun, Hui‐Ling</au><au>Liu, Xiang‐Xiang</au><au>Xu, Xue‐Ni</au><au>Chen, Xiao‐Xiang</au><au>Zeng, Kai‐Xuan</au><au>Xu, Mu</au><au>Wang, Shu‐Kui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR‐142‐3p functions as a tumor suppressor by targeting RAC1/PAK1 pathway in breast cancer</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2020-05</date><risdate>2020</risdate><volume>235</volume><issue>5</issue><spage>4928</spage><epage>4940</epage><pages>4928-4940</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>MicroRNA‐142‐3p (miR‐142‐3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR‐142‐3p was markedly decreased both in cell lines and BC tumor tissues. Elevated miR‐142‐3p expression suppressed growth and metastasis of BC cell lines via gain‐of‐function assay in vitro and in vivo. Mechanistically, miR‐142‐3p could regulate the ras‐related C3 botulinum toxin substrate 1 (RAC1) expression in protein level, which simultaneously suppressed the epithelial‐to‐mesenchymal transition related protein levels and the activity of PAK1 phosphorylation, respectively. In addition, rescue experiments revealed RAC1 overexpression could reverse tumor‐suppressive role of miR‐142‐3p. Our results showed miR‐142‐3p could function as a tumor suppressor via targeting RAC1/PAK1 pathway in BC, suggesting a potent therapeutic target for BC treatment.
MiR‐142‐3p is downregulated in breast cancer (BC) tissues and cell lines. MiR‐142‐3p may act as a tumor suppressor by regulating cell proliferation, migration, invasion, angiogenesis, and epithelial‐to‐mesenchymal transition process through directly downregulation of ras‐related C3 botulinum toxin substrate 1 expression and subsequently inhibiting the activity of PAK1 phosphorylation in BC.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31674013</pmid><doi>10.1002/jcp.29372</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-6972-2587</orcidid></addata></record> |
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| subjects | Animals Apoptosis Biotechnology Botulinum toxin Breast cancer Breast Neoplasms - enzymology Breast Neoplasms - genetics Breast Neoplasms - pathology Cell Movement Cell Proliferation Databases, Genetic Female Gene Expression Regulation, Neoplastic Humans MCF-7 Cells Mesenchyme Metastases Mice, Inbred BALB C Mice, Nude MicroRNAs - genetics MicroRNAs - metabolism miRNA miR‐142‐3p Neoplasm Invasiveness Neovascularization, Pathologic p21-Activated Kinases - genetics p21-Activated Kinases - metabolism PAK1 Phosphorylation Proteins RAC1 rac1 GTP-Binding Protein - genetics rac1 GTP-Binding Protein - metabolism Rac1 protein Signal Transduction Substrates Therapeutic applications Toxins Tumor cell lines Tumor suppressor genes Tumors |
| title | MiR‐142‐3p functions as a tumor suppressor by targeting RAC1/PAK1 pathway in breast cancer |
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