VCAM-1 secreted from cancer-associated fibroblasts enhances the growth and invasion of lung cancer cells through AKT and MAPK signaling
Several studies have indicated that cancer-associated fibroblasts (CAFs) could promote cancer progression in many malignancies. However, the mechanism by which CAFs promote the growth and metastasis of lung cancer remains poorly defined. In the present study, CAFs and normal fibroblasts (NFs) were i...
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| Veröffentlicht in: | Cancer letters 2020-03, Vol.473, p.62-73 |
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| container_title | Cancer letters |
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| creator | Zhou, Zhuan Zhou, Qin Wu, Xia Xu, San Hu, Xiaohong Tao, Xuxiu Li, Bo Peng, Jinwu Li, Dan Shen, Liangfang Cao, Ya Yang, Lifang |
| description | Several studies have indicated that cancer-associated fibroblasts (CAFs) could promote cancer progression in many malignancies. However, the mechanism by which CAFs promote the growth and metastasis of lung cancer remains poorly defined. In the present study, CAFs and normal fibroblasts (NFs) were isolated from human lung cancer and adjacent tissue. The data showed that the conditional medium (CM) of CAFs could increase the proliferation, migration and invasion of lung cancer cells. Vascular cell adhesion molecule-1 (VCAM-1) showed a higher expression in CAF-CM than NF-CM, and blocking VCAM-1 in CAF-CM attenuated the proliferation and invasion of cancer cells. Further, the results showed that VCAM-1 secreted from CAFs activated AKT and MAPK signaling via receptor α4β1 integrin (very-late antigen (VLA)-4) in lung cancer cells. Moreover, CAFs promoted VCAM-1 expression and tumor growth in vivo. Additionally, bioinformatics analysis indicated a positive correlation on the CAF marker protein alpha-smooth muscle actin (α-SMA) and VCAM-1 expression, which was associated with a poor prognosis in lung cancer patients. These findings demonstrate that the VCAM-1 secreted from CAFs enhances growth and invasion by activating the AKT and MAPK signaling of lung cancer cells.
•VCAM-1secreted from cancer associated fibroblasts (CAFs) promotes lung cancer cells proliferation, migration and invasion.•CAFs activated AKT and MAPK signaling via VCAM-1 receptor very-late antigen (VLA)-4 in lung cancer cells.•VCAM-1 expression was associated with a poor prognosis in lung cancer patients. |
| doi_str_mv | 10.1016/j.canlet.2019.12.039 |
| format | Article |
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•VCAM-1secreted from cancer associated fibroblasts (CAFs) promotes lung cancer cells proliferation, migration and invasion.•CAFs activated AKT and MAPK signaling via VCAM-1 receptor very-late antigen (VLA)-4 in lung cancer cells.•VCAM-1 expression was associated with a poor prognosis in lung cancer patients.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2019.12.039</identifier><identifier>PMID: 31904479</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Actin ; AKT ; AKT protein ; Arrays ; Bioinformatics ; Cancer invasion ; Cancer therapies ; Cancer-associated fibroblasts ; Cell adhesion ; Cell adhesion & migration ; Cell adhesion molecules ; Cell culture ; Cell proliferation ; Cytokines ; Fibroblasts ; Immunoglobulins ; Insulin-like growth factors ; Lung cancer ; MAP kinase ; MAPK ; Medical prognosis ; Metastases ; Metastasis ; Muscles ; Proteins ; R&D ; Research & development ; Smooth muscle ; Vascular cell adhesion molecule 1</subject><ispartof>Cancer letters, 2020-03, Vol.473, p.62-73</ispartof><rights>2020 Elsevier B.V.</rights><rights>Copyright © 2020 Elsevier B.V. All rights reserved.</rights><rights>2020. Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-6c3d2f69d3cffd908ba60f8228d50aa9595627e1ead0b18662a263145d0abdb63</citedby><cites>FETCH-LOGICAL-c390t-6c3d2f69d3cffd908ba60f8228d50aa9595627e1ead0b18662a263145d0abdb63</cites><orcidid>0000-0002-3012-8350</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2019.12.039$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31904479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Zhuan</creatorcontrib><creatorcontrib>Zhou, Qin</creatorcontrib><creatorcontrib>Wu, Xia</creatorcontrib><creatorcontrib>Xu, San</creatorcontrib><creatorcontrib>Hu, Xiaohong</creatorcontrib><creatorcontrib>Tao, Xuxiu</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Peng, Jinwu</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Shen, Liangfang</creatorcontrib><creatorcontrib>Cao, Ya</creatorcontrib><creatorcontrib>Yang, Lifang</creatorcontrib><title>VCAM-1 secreted from cancer-associated fibroblasts enhances the growth and invasion of lung cancer cells through AKT and MAPK signaling</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Several studies have indicated that cancer-associated fibroblasts (CAFs) could promote cancer progression in many malignancies. However, the mechanism by which CAFs promote the growth and metastasis of lung cancer remains poorly defined. In the present study, CAFs and normal fibroblasts (NFs) were isolated from human lung cancer and adjacent tissue. The data showed that the conditional medium (CM) of CAFs could increase the proliferation, migration and invasion of lung cancer cells. Vascular cell adhesion molecule-1 (VCAM-1) showed a higher expression in CAF-CM than NF-CM, and blocking VCAM-1 in CAF-CM attenuated the proliferation and invasion of cancer cells. Further, the results showed that VCAM-1 secreted from CAFs activated AKT and MAPK signaling via receptor α4β1 integrin (very-late antigen (VLA)-4) in lung cancer cells. Moreover, CAFs promoted VCAM-1 expression and tumor growth in vivo. Additionally, bioinformatics analysis indicated a positive correlation on the CAF marker protein alpha-smooth muscle actin (α-SMA) and VCAM-1 expression, which was associated with a poor prognosis in lung cancer patients. These findings demonstrate that the VCAM-1 secreted from CAFs enhances growth and invasion by activating the AKT and MAPK signaling of lung cancer cells.
•VCAM-1secreted from cancer associated fibroblasts (CAFs) promotes lung cancer cells proliferation, migration and invasion.•CAFs activated AKT and MAPK signaling via VCAM-1 receptor very-late antigen (VLA)-4 in lung cancer cells.•VCAM-1 expression was associated with a poor prognosis in lung cancer patients.</description><subject>Actin</subject><subject>AKT</subject><subject>AKT protein</subject><subject>Arrays</subject><subject>Bioinformatics</subject><subject>Cancer invasion</subject><subject>Cancer therapies</subject><subject>Cancer-associated fibroblasts</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell culture</subject><subject>Cell proliferation</subject><subject>Cytokines</subject><subject>Fibroblasts</subject><subject>Immunoglobulins</subject><subject>Insulin-like growth factors</subject><subject>Lung cancer</subject><subject>MAP kinase</subject><subject>MAPK</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Muscles</subject><subject>Proteins</subject><subject>R&D</subject><subject>Research & development</subject><subject>Smooth muscle</subject><subject>Vascular cell adhesion molecule 1</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kMFO3DAURa2qqAy0f4CQpa4Tnu3EiTeVRiNoEaB2Qbu1HPsl41EmpnYC6hfw280wA0tWT_I799o-hJwxyBkwebHJrRl6HHMOTOWM5yDUB7JgdcWzStXwkSxAQJGJWpTH5CSlDQCURVV-IseCKSiKSi3I85_V8i5jNKGNOKKjbQxbOjdbjJlJKVhvXo59E0PTmzQmisN6t090XCPtYnga19QMjvrh0SQfBhpa2k9Dd6ihFvt-B8cwdWu6vLl_oe-Wv25o8t1gej90n8lRa_qEXw7zlPy-urxf_chuf36_Xi1vMysUjJm0wvFWKids2zoFdWMktDXntSvBGFWqUvIKGRoHDaul5IZLwYrSgWlcI8Up-brvfYjh74Rp1JswxfkNSXNRcK6ghHqmij1lY0gpYqsfot-a-E8z0Dv7eqP39vXOvmZcz_bn2PmhfGq26N5Cr7pn4NsewPmLjx6jTtbjLMn5iHbULvj3b_gPNUyYaw</recordid><startdate>20200331</startdate><enddate>20200331</enddate><creator>Zhou, Zhuan</creator><creator>Zhou, Qin</creator><creator>Wu, Xia</creator><creator>Xu, San</creator><creator>Hu, Xiaohong</creator><creator>Tao, Xuxiu</creator><creator>Li, Bo</creator><creator>Peng, Jinwu</creator><creator>Li, Dan</creator><creator>Shen, Liangfang</creator><creator>Cao, Ya</creator><creator>Yang, Lifang</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><orcidid>https://orcid.org/0000-0002-3012-8350</orcidid></search><sort><creationdate>20200331</creationdate><title>VCAM-1 secreted from cancer-associated fibroblasts enhances the growth and invasion of lung cancer cells through AKT and MAPK signaling</title><author>Zhou, Zhuan ; Zhou, Qin ; Wu, Xia ; Xu, San ; Hu, Xiaohong ; Tao, Xuxiu ; Li, Bo ; Peng, Jinwu ; Li, Dan ; Shen, Liangfang ; Cao, Ya ; Yang, Lifang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-6c3d2f69d3cffd908ba60f8228d50aa9595627e1ead0b18662a263145d0abdb63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Actin</topic><topic>AKT</topic><topic>AKT protein</topic><topic>Arrays</topic><topic>Bioinformatics</topic><topic>Cancer invasion</topic><topic>Cancer therapies</topic><topic>Cancer-associated fibroblasts</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell adhesion molecules</topic><topic>Cell culture</topic><topic>Cell proliferation</topic><topic>Cytokines</topic><topic>Fibroblasts</topic><topic>Immunoglobulins</topic><topic>Insulin-like growth factors</topic><topic>Lung cancer</topic><topic>MAP kinase</topic><topic>MAPK</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Muscles</topic><topic>Proteins</topic><topic>R&D</topic><topic>Research & development</topic><topic>Smooth muscle</topic><topic>Vascular cell adhesion molecule 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Zhuan</creatorcontrib><creatorcontrib>Zhou, Qin</creatorcontrib><creatorcontrib>Wu, Xia</creatorcontrib><creatorcontrib>Xu, San</creatorcontrib><creatorcontrib>Hu, Xiaohong</creatorcontrib><creatorcontrib>Tao, Xuxiu</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Peng, Jinwu</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Shen, Liangfang</creatorcontrib><creatorcontrib>Cao, Ya</creatorcontrib><creatorcontrib>Yang, Lifang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Zhuan</au><au>Zhou, Qin</au><au>Wu, Xia</au><au>Xu, San</au><au>Hu, Xiaohong</au><au>Tao, Xuxiu</au><au>Li, Bo</au><au>Peng, Jinwu</au><au>Li, Dan</au><au>Shen, Liangfang</au><au>Cao, Ya</au><au>Yang, Lifang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>VCAM-1 secreted from cancer-associated fibroblasts enhances the growth and invasion of lung cancer cells through AKT and MAPK signaling</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2020-03-31</date><risdate>2020</risdate><volume>473</volume><spage>62</spage><epage>73</epage><pages>62-73</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Several studies have indicated that cancer-associated fibroblasts (CAFs) could promote cancer progression in many malignancies. However, the mechanism by which CAFs promote the growth and metastasis of lung cancer remains poorly defined. In the present study, CAFs and normal fibroblasts (NFs) were isolated from human lung cancer and adjacent tissue. The data showed that the conditional medium (CM) of CAFs could increase the proliferation, migration and invasion of lung cancer cells. Vascular cell adhesion molecule-1 (VCAM-1) showed a higher expression in CAF-CM than NF-CM, and blocking VCAM-1 in CAF-CM attenuated the proliferation and invasion of cancer cells. Further, the results showed that VCAM-1 secreted from CAFs activated AKT and MAPK signaling via receptor α4β1 integrin (very-late antigen (VLA)-4) in lung cancer cells. Moreover, CAFs promoted VCAM-1 expression and tumor growth in vivo. Additionally, bioinformatics analysis indicated a positive correlation on the CAF marker protein alpha-smooth muscle actin (α-SMA) and VCAM-1 expression, which was associated with a poor prognosis in lung cancer patients. These findings demonstrate that the VCAM-1 secreted from CAFs enhances growth and invasion by activating the AKT and MAPK signaling of lung cancer cells.
•VCAM-1secreted from cancer associated fibroblasts (CAFs) promotes lung cancer cells proliferation, migration and invasion.•CAFs activated AKT and MAPK signaling via VCAM-1 receptor very-late antigen (VLA)-4 in lung cancer cells.•VCAM-1 expression was associated with a poor prognosis in lung cancer patients.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>31904479</pmid><doi>10.1016/j.canlet.2019.12.039</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-3012-8350</orcidid></addata></record> |
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| subjects | Actin AKT AKT protein Arrays Bioinformatics Cancer invasion Cancer therapies Cancer-associated fibroblasts Cell adhesion Cell adhesion & migration Cell adhesion molecules Cell culture Cell proliferation Cytokines Fibroblasts Immunoglobulins Insulin-like growth factors Lung cancer MAP kinase MAPK Medical prognosis Metastases Metastasis Muscles Proteins R&D Research & development Smooth muscle Vascular cell adhesion molecule 1 |
| title | VCAM-1 secreted from cancer-associated fibroblasts enhances the growth and invasion of lung cancer cells through AKT and MAPK signaling |
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