Loading…
Activation of fibroblasts by nicotine promotes the epithelial‐mesenchymal transition and motility of breast cancer cells
The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking‐related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotin...
Saved in:
| Published in: | Journal of cellular physiology 2018-06, Vol.233 (6), p.4972-4980 |
|---|---|
| Main Authors: | , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3 |
| container_end_page | 4980 |
| container_issue | 6 |
| container_start_page | 4972 |
| container_title | Journal of cellular physiology |
| container_volume | 233 |
| creator | Chen, Pin‐Cyuan Lee, Wen‐Ying Ling, Hsiang‐Hsi Cheng, Chia‐Hsiung Chen, Ku‐Chung Lin, Cheng‐Wei |
| description | The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking‐related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotine‐mediated tumorigenesis is poorly understood. Herein, we investigated the effect and molecular mechanism of nicotine on fibroblasts and its contribution to breast cancer. We found that nicotine induced the epithelial‐mesenchymal transition (EMT) of breast cancer cells and promoted activation of fibroblasts. Interestingly, conditioned medium from nicotine‐activated fibroblasts (Nic–CM) had a greater impact on promoting the EMT and migratory capability toward cancer cells than did treatment with nicotine alone. Production of connective tissue growth factor (CTGF) and transforming growth factor (TGF)‐β by nicotine‐treated fibroblasts was demonstrated to be crucial for promoting the EMT and cancer cell migration, and blocking of CTGF and TGF‐β in Nic‐CM‐suppressed tumor motility. Moreover, nicotine induced expressions of CTGF, and TGF‐β in fibroblasts as identified through α7 nicotinic acetylcholine receptor (nAChR)‐dependent activation of the AKT/TAZ signaling mechanism. Together, our data showed for the first time that activation of fibroblasts is largely responsible for accelerating smoking‐mediated breast cancer progression.
Nicotine mediates production of CTGF and TGFβ in fibroblasts through α7 nAChR‐dependent activation of AKT/TAZ signaling, which further promotes EMT, and motility of breast cancer. |
| doi_str_mv | 10.1002/jcp.26334 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1974000239</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1974000239</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3</originalsourceid><addsrcrecordid>eNp1kbtOHDEUhq0IFDaQghdAlmiSYsCXmfG4RCtyExIpQm3Z3jPCK4-92N5EQ5VHyDPmSeJlSYpIVKc4nz_9xz9Cp5RcUELY5dpuLljPefsKLSiRomn7jh2gRd3RRnYtPUJvcl4TQqTk_DU6YpLRTpBugR6vbHHfdXEx4Dji0ZkUjde5ZGxmHJyNxQXAmxSnWCDjcg8YNq4O77T__fPXBBmCvZ8n7XFJOmT35NJhhesL512Zd2KToEqx1cFCwha8zyfocNQ-w9vneYzuPlx_W35qbm4_fl5e3TS2pbJtVpTLngluOWkHOdbkYMaupystKGijOedEWy7lAKKXHRVUjsT2Q6uFpsIYfoze7b31iIct5KIml3cJdIC4zYpK0davYVxW9Pw_dB23KdR0ihEysKGj_VCp93vKpphzglFtkpt0mhUlaleIqoWop0Iqe_Zs3JoJVv_Ivw1U4HIP_HAe5pdN6svy6175B3kGlr4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2008285168</pqid></control><display><type>article</type><title>Activation of fibroblasts by nicotine promotes the epithelial‐mesenchymal transition and motility of breast cancer cells</title><source>Wiley</source><creator>Chen, Pin‐Cyuan ; Lee, Wen‐Ying ; Ling, Hsiang‐Hsi ; Cheng, Chia‐Hsiung ; Chen, Ku‐Chung ; Lin, Cheng‐Wei</creator><creatorcontrib>Chen, Pin‐Cyuan ; Lee, Wen‐Ying ; Ling, Hsiang‐Hsi ; Cheng, Chia‐Hsiung ; Chen, Ku‐Chung ; Lin, Cheng‐Wei</creatorcontrib><description>The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking‐related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotine‐mediated tumorigenesis is poorly understood. Herein, we investigated the effect and molecular mechanism of nicotine on fibroblasts and its contribution to breast cancer. We found that nicotine induced the epithelial‐mesenchymal transition (EMT) of breast cancer cells and promoted activation of fibroblasts. Interestingly, conditioned medium from nicotine‐activated fibroblasts (Nic–CM) had a greater impact on promoting the EMT and migratory capability toward cancer cells than did treatment with nicotine alone. Production of connective tissue growth factor (CTGF) and transforming growth factor (TGF)‐β by nicotine‐treated fibroblasts was demonstrated to be crucial for promoting the EMT and cancer cell migration, and blocking of CTGF and TGF‐β in Nic‐CM‐suppressed tumor motility. Moreover, nicotine induced expressions of CTGF, and TGF‐β in fibroblasts as identified through α7 nicotinic acetylcholine receptor (nAChR)‐dependent activation of the AKT/TAZ signaling mechanism. Together, our data showed for the first time that activation of fibroblasts is largely responsible for accelerating smoking‐mediated breast cancer progression.
Nicotine mediates production of CTGF and TGFβ in fibroblasts through α7 nAChR‐dependent activation of AKT/TAZ signaling, which further promotes EMT, and motility of breast cancer.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.26334</identifier><identifier>PMID: 29215705</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acetylcholine receptors (nicotinic) ; Activation ; AKT protein ; alpha7 Nicotinic Acetylcholine Receptor - agonists ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer ; Cancer-Associated Fibroblasts - drug effects ; Cancer-Associated Fibroblasts - metabolism ; Cancer-Associated Fibroblasts - pathology ; Carcinogens - toxicity ; Cell migration ; Cell Movement - drug effects ; Cigarette smoking ; Conditioning ; Connective tissue growth factor ; Connective Tissue Growth Factor - metabolism ; Connective tissues ; Culture Media, Conditioned - metabolism ; EMT ; Epithelial-Mesenchymal Transition - drug effects ; Female ; Fibroblasts ; Growth factors ; Humans ; Intracellular Signaling Peptides and Proteins - metabolism ; MCF-7 Cells ; Mesenchyme ; Motility ; Neoplasm Invasiveness ; Nicotine ; Nicotine - toxicity ; Paracrine Communication - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; Signaling ; Smoking ; Smoking - adverse effects ; Transforming Growth Factor beta - metabolism ; Tumor cells ; Tumor Microenvironment ; Tumorigenesis</subject><ispartof>Journal of cellular physiology, 2018-06, Vol.233 (6), p.4972-4980</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3</citedby><cites>FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3</cites><orcidid>0000-0003-4622-2680</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.26334$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.26334$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29215705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Pin‐Cyuan</creatorcontrib><creatorcontrib>Lee, Wen‐Ying</creatorcontrib><creatorcontrib>Ling, Hsiang‐Hsi</creatorcontrib><creatorcontrib>Cheng, Chia‐Hsiung</creatorcontrib><creatorcontrib>Chen, Ku‐Chung</creatorcontrib><creatorcontrib>Lin, Cheng‐Wei</creatorcontrib><title>Activation of fibroblasts by nicotine promotes the epithelial‐mesenchymal transition and motility of breast cancer cells</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking‐related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotine‐mediated tumorigenesis is poorly understood. Herein, we investigated the effect and molecular mechanism of nicotine on fibroblasts and its contribution to breast cancer. We found that nicotine induced the epithelial‐mesenchymal transition (EMT) of breast cancer cells and promoted activation of fibroblasts. Interestingly, conditioned medium from nicotine‐activated fibroblasts (Nic–CM) had a greater impact on promoting the EMT and migratory capability toward cancer cells than did treatment with nicotine alone. Production of connective tissue growth factor (CTGF) and transforming growth factor (TGF)‐β by nicotine‐treated fibroblasts was demonstrated to be crucial for promoting the EMT and cancer cell migration, and blocking of CTGF and TGF‐β in Nic‐CM‐suppressed tumor motility. Moreover, nicotine induced expressions of CTGF, and TGF‐β in fibroblasts as identified through α7 nicotinic acetylcholine receptor (nAChR)‐dependent activation of the AKT/TAZ signaling mechanism. Together, our data showed for the first time that activation of fibroblasts is largely responsible for accelerating smoking‐mediated breast cancer progression.
Nicotine mediates production of CTGF and TGFβ in fibroblasts through α7 nAChR‐dependent activation of AKT/TAZ signaling, which further promotes EMT, and motility of breast cancer.</description><subject>Acetylcholine receptors (nicotinic)</subject><subject>Activation</subject><subject>AKT protein</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - agonists</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Cancer-Associated Fibroblasts - drug effects</subject><subject>Cancer-Associated Fibroblasts - metabolism</subject><subject>Cancer-Associated Fibroblasts - pathology</subject><subject>Carcinogens - toxicity</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cigarette smoking</subject><subject>Conditioning</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Connective tissues</subject><subject>Culture Media, Conditioned - metabolism</subject><subject>EMT</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>MCF-7 Cells</subject><subject>Mesenchyme</subject><subject>Motility</subject><subject>Neoplasm Invasiveness</subject><subject>Nicotine</subject><subject>Nicotine - toxicity</subject><subject>Paracrine Communication - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Smoking</subject><subject>Smoking - adverse effects</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Tumor cells</subject><subject>Tumor Microenvironment</subject><subject>Tumorigenesis</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kbtOHDEUhq0IFDaQghdAlmiSYsCXmfG4RCtyExIpQm3Z3jPCK4-92N5EQ5VHyDPmSeJlSYpIVKc4nz_9xz9Cp5RcUELY5dpuLljPefsKLSiRomn7jh2gRd3RRnYtPUJvcl4TQqTk_DU6YpLRTpBugR6vbHHfdXEx4Dji0ZkUjde5ZGxmHJyNxQXAmxSnWCDjcg8YNq4O77T__fPXBBmCvZ8n7XFJOmT35NJhhesL512Zd2KToEqx1cFCwha8zyfocNQ-w9vneYzuPlx_W35qbm4_fl5e3TS2pbJtVpTLngluOWkHOdbkYMaupystKGijOedEWy7lAKKXHRVUjsT2Q6uFpsIYfoze7b31iIct5KIml3cJdIC4zYpK0davYVxW9Pw_dB23KdR0ihEysKGj_VCp93vKpphzglFtkpt0mhUlaleIqoWop0Iqe_Zs3JoJVv_Ivw1U4HIP_HAe5pdN6svy6175B3kGlr4</recordid><startdate>201806</startdate><enddate>201806</enddate><creator>Chen, Pin‐Cyuan</creator><creator>Lee, Wen‐Ying</creator><creator>Ling, Hsiang‐Hsi</creator><creator>Cheng, Chia‐Hsiung</creator><creator>Chen, Ku‐Chung</creator><creator>Lin, Cheng‐Wei</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/0000-0003-4622-2680</orcidid></search><sort><creationdate>201806</creationdate><title>Activation of fibroblasts by nicotine promotes the epithelial‐mesenchymal transition and motility of breast cancer cells</title><author>Chen, Pin‐Cyuan ; Lee, Wen‐Ying ; Ling, Hsiang‐Hsi ; Cheng, Chia‐Hsiung ; Chen, Ku‐Chung ; Lin, Cheng‐Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetylcholine receptors (nicotinic)</topic><topic>Activation</topic><topic>AKT protein</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - agonists</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer</topic><topic>Cancer-Associated Fibroblasts - drug effects</topic><topic>Cancer-Associated Fibroblasts - metabolism</topic><topic>Cancer-Associated Fibroblasts - pathology</topic><topic>Carcinogens - toxicity</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cigarette smoking</topic><topic>Conditioning</topic><topic>Connective tissue growth factor</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Connective tissues</topic><topic>Culture Media, Conditioned - metabolism</topic><topic>EMT</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>MCF-7 Cells</topic><topic>Mesenchyme</topic><topic>Motility</topic><topic>Neoplasm Invasiveness</topic><topic>Nicotine</topic><topic>Nicotine - toxicity</topic><topic>Paracrine Communication - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Smoking</topic><topic>Smoking - adverse effects</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Tumor cells</topic><topic>Tumor Microenvironment</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Pin‐Cyuan</creatorcontrib><creatorcontrib>Lee, Wen‐Ying</creatorcontrib><creatorcontrib>Ling, Hsiang‐Hsi</creatorcontrib><creatorcontrib>Cheng, Chia‐Hsiung</creatorcontrib><creatorcontrib>Chen, Ku‐Chung</creatorcontrib><creatorcontrib>Lin, Cheng‐Wei</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>Chen, Pin‐Cyuan</au><au>Lee, Wen‐Ying</au><au>Ling, Hsiang‐Hsi</au><au>Cheng, Chia‐Hsiung</au><au>Chen, Ku‐Chung</au><au>Lin, Cheng‐Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of fibroblasts by nicotine promotes the epithelial‐mesenchymal transition and motility of breast cancer cells</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2018-06</date><risdate>2018</risdate><volume>233</volume><issue>6</issue><spage>4972</spage><epage>4980</epage><pages>4972-4980</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking‐related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotine‐mediated tumorigenesis is poorly understood. Herein, we investigated the effect and molecular mechanism of nicotine on fibroblasts and its contribution to breast cancer. We found that nicotine induced the epithelial‐mesenchymal transition (EMT) of breast cancer cells and promoted activation of fibroblasts. Interestingly, conditioned medium from nicotine‐activated fibroblasts (Nic–CM) had a greater impact on promoting the EMT and migratory capability toward cancer cells than did treatment with nicotine alone. Production of connective tissue growth factor (CTGF) and transforming growth factor (TGF)‐β by nicotine‐treated fibroblasts was demonstrated to be crucial for promoting the EMT and cancer cell migration, and blocking of CTGF and TGF‐β in Nic‐CM‐suppressed tumor motility. Moreover, nicotine induced expressions of CTGF, and TGF‐β in fibroblasts as identified through α7 nicotinic acetylcholine receptor (nAChR)‐dependent activation of the AKT/TAZ signaling mechanism. Together, our data showed for the first time that activation of fibroblasts is largely responsible for accelerating smoking‐mediated breast cancer progression.
Nicotine mediates production of CTGF and TGFβ in fibroblasts through α7 nAChR‐dependent activation of AKT/TAZ signaling, which further promotes EMT, and motility of breast cancer.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29215705</pmid><doi>10.1002/jcp.26334</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-4622-2680</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9541 |
| ispartof | Journal of cellular physiology, 2018-06, Vol.233 (6), p.4972-4980 |
| issn | 0021-9541 1097-4652 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1974000239 |
| source | Wiley |
| subjects | Acetylcholine receptors (nicotinic) Activation AKT protein alpha7 Nicotinic Acetylcholine Receptor - agonists alpha7 Nicotinic Acetylcholine Receptor - metabolism Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Cancer-Associated Fibroblasts - drug effects Cancer-Associated Fibroblasts - metabolism Cancer-Associated Fibroblasts - pathology Carcinogens - toxicity Cell migration Cell Movement - drug effects Cigarette smoking Conditioning Connective tissue growth factor Connective Tissue Growth Factor - metabolism Connective tissues Culture Media, Conditioned - metabolism EMT Epithelial-Mesenchymal Transition - drug effects Female Fibroblasts Growth factors Humans Intracellular Signaling Peptides and Proteins - metabolism MCF-7 Cells Mesenchyme Motility Neoplasm Invasiveness Nicotine Nicotine - toxicity Paracrine Communication - drug effects Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects Signaling Smoking Smoking - adverse effects Transforming Growth Factor beta - metabolism Tumor cells Tumor Microenvironment Tumorigenesis |
| title | Activation of fibroblasts by nicotine promotes the epithelial‐mesenchymal transition and motility of breast cancer cells |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-23T01%3A30%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Activation%20of%20fibroblasts%20by%20nicotine%20promotes%20the%20epithelial%E2%80%90mesenchymal%20transition%20and%20motility%20of%20breast%20cancer%20cells&rft.jtitle=Journal%20of%20cellular%20physiology&rft.au=Chen,%20Pin%E2%80%90Cyuan&rft.date=2018-06&rft.volume=233&rft.issue=6&rft.spage=4972&rft.epage=4980&rft.pages=4972-4980&rft.issn=0021-9541&rft.eissn=1097-4652&rft_id=info:doi/10.1002/jcp.26334&rft_dat=%3Cproquest_cross%3E1974000239%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4194-d1396273c30489f921ebf561da71eaba3330ac3998e76951719f0c684a7a17bb3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2008285168&rft_id=info:pmid/29215705&rfr_iscdi=true |