Increased T‐helper 17 cell differentiation mediated by exosome‐mediated micro RNA ‐451 redistribution in gastric cancer infiltrated T cells
Micro RNA (miR)‐451 is a cell metabolism‐related mi RNA that can mediate cell energy‐consuming models by several targets. As miR‐451 can promote mechanistic target of rapamycin ( mTOR ) activity, and increased mTOR activity is related to increased differentiation of T‐helper 17 (Th17) cells, we soug...
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| Veröffentlicht in: | Cancer science 2018-01, Vol.109 (1), p.65-73 |
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| creator | Liu, Feng Bu, Zhouyan Zhao, Feng Xiao, Daping |
| description | Micro
RNA
(miR)‐451 is a cell metabolism‐related mi
RNA
that can mediate cell energy‐consuming models by several targets. As miR‐451 can promote mechanistic target of rapamycin (
mTOR
) activity, and increased
mTOR
activity is related to increased differentiation of T‐helper 17 (Th17) cells, we sought to investigate whether miR‐451 can redistribute from cancer cells to infiltrated T cells and enhance the distribution of Th17 cells through
mTOR
. Real‐time
PCR
was used for detecting expression of miR‐451 in gastric cancer, tumor infiltrated T cells and exosomes, and distribution of Th17 was evaluated by both flow cytometry and immunohistochemistry (
IHC
). Immunofluorescence staining was used in monitoring the exosome‐enveloped miR‐451 from cancer cells to T cells with different treatments, and signaling pathway change was analyzed by western blot. miR‐451 decreased significantly in gastric cancer (
GC
) tissues but increased in infiltrated T cells and exosomes; tumor miR‐451 was negatively related to infiltrated T cells and exosome miR‐451. Exosome miR‐451 can not only serve as an indicator for poor prognosis of post‐operation
GC
patients but is also related to increased Th17 distribution in gastric cancer. miR‐451 can redistribute from cancer cells to T cells with low glucose treatment. Decreased 5′
AMP
‐activated protein kinase (
AMPK
) and increased
mTOR
activity was investigated in miR‐451 redistributed T cells and the Th17 polarized differentiation of these T cells were also increased. Exosome miR‐451 derived from tumor tissues can serve as an indicator for poor prognosis and redistribution of miR‐451 from cancer cells to infiltrated T cells in low glucose treatment can enhance Th17 differentiation by enhancing
mTOR
activity. |
| doi_str_mv | 10.1111/cas.13429 |
| format | Article |
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RNA
(miR)‐451 is a cell metabolism‐related mi
RNA
that can mediate cell energy‐consuming models by several targets. As miR‐451 can promote mechanistic target of rapamycin (
mTOR
) activity, and increased
mTOR
activity is related to increased differentiation of T‐helper 17 (Th17) cells, we sought to investigate whether miR‐451 can redistribute from cancer cells to infiltrated T cells and enhance the distribution of Th17 cells through
mTOR
. Real‐time
PCR
was used for detecting expression of miR‐451 in gastric cancer, tumor infiltrated T cells and exosomes, and distribution of Th17 was evaluated by both flow cytometry and immunohistochemistry (
IHC
). Immunofluorescence staining was used in monitoring the exosome‐enveloped miR‐451 from cancer cells to T cells with different treatments, and signaling pathway change was analyzed by western blot. miR‐451 decreased significantly in gastric cancer (
GC
) tissues but increased in infiltrated T cells and exosomes; tumor miR‐451 was negatively related to infiltrated T cells and exosome miR‐451. Exosome miR‐451 can not only serve as an indicator for poor prognosis of post‐operation
GC
patients but is also related to increased Th17 distribution in gastric cancer. miR‐451 can redistribute from cancer cells to T cells with low glucose treatment. Decreased 5′
AMP
‐activated protein kinase (
AMPK
) and increased
mTOR
activity was investigated in miR‐451 redistributed T cells and the Th17 polarized differentiation of these T cells were also increased. Exosome miR‐451 derived from tumor tissues can serve as an indicator for poor prognosis and redistribution of miR‐451 from cancer cells to infiltrated T cells in low glucose treatment can enhance Th17 differentiation by enhancing
mTOR
activity.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.13429</identifier><language>eng</language><publisher>Tokyo: John Wiley & Sons, Inc</publisher><subject>AMP ; Apoptosis ; Blood ; Cell culture ; Cell differentiation ; Cell growth ; Exosomes ; Flow cytometry ; Gastric cancer ; Helper cells ; Immunofluorescence ; Immunohistochemistry ; Leukemia ; Lymphocytes ; Lymphocytes T ; Medical prognosis ; Medical research ; Metastasis ; MicroRNAs ; miRNA ; Prognosis ; Protein kinase ; Proteins ; Rapamycin ; Signal transduction ; Studies ; Surgery ; TOR protein</subject><ispartof>Cancer science, 2018-01, Vol.109 (1), p.65-73</ispartof><rights>2018. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1022-fc56c8b77a6ed5065d178a52e822e47e31ccf2a251e1bf995b8602834dc1af853</citedby><cites>FETCH-LOGICAL-c1022-fc56c8b77a6ed5065d178a52e822e47e31ccf2a251e1bf995b8602834dc1af853</cites><orcidid>0000-0003-4422-6389</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids></links><search><creatorcontrib>Liu, Feng</creatorcontrib><creatorcontrib>Bu, Zhouyan</creatorcontrib><creatorcontrib>Zhao, Feng</creatorcontrib><creatorcontrib>Xiao, Daping</creatorcontrib><title>Increased T‐helper 17 cell differentiation mediated by exosome‐mediated micro RNA ‐451 redistribution in gastric cancer infiltrated T cells</title><title>Cancer science</title><description>Micro
RNA
(miR)‐451 is a cell metabolism‐related mi
RNA
that can mediate cell energy‐consuming models by several targets. As miR‐451 can promote mechanistic target of rapamycin (
mTOR
) activity, and increased
mTOR
activity is related to increased differentiation of T‐helper 17 (Th17) cells, we sought to investigate whether miR‐451 can redistribute from cancer cells to infiltrated T cells and enhance the distribution of Th17 cells through
mTOR
. Real‐time
PCR
was used for detecting expression of miR‐451 in gastric cancer, tumor infiltrated T cells and exosomes, and distribution of Th17 was evaluated by both flow cytometry and immunohistochemistry (
IHC
). Immunofluorescence staining was used in monitoring the exosome‐enveloped miR‐451 from cancer cells to T cells with different treatments, and signaling pathway change was analyzed by western blot. miR‐451 decreased significantly in gastric cancer (
GC
) tissues but increased in infiltrated T cells and exosomes; tumor miR‐451 was negatively related to infiltrated T cells and exosome miR‐451. Exosome miR‐451 can not only serve as an indicator for poor prognosis of post‐operation
GC
patients but is also related to increased Th17 distribution in gastric cancer. miR‐451 can redistribute from cancer cells to T cells with low glucose treatment. Decreased 5′
AMP
‐activated protein kinase (
AMPK
) and increased
mTOR
activity was investigated in miR‐451 redistributed T cells and the Th17 polarized differentiation of these T cells were also increased. Exosome miR‐451 derived from tumor tissues can serve as an indicator for poor prognosis and redistribution of miR‐451 from cancer cells to infiltrated T cells in low glucose treatment can enhance Th17 differentiation by enhancing
mTOR
activity.</description><subject>AMP</subject><subject>Apoptosis</subject><subject>Blood</subject><subject>Cell culture</subject><subject>Cell differentiation</subject><subject>Cell growth</subject><subject>Exosomes</subject><subject>Flow cytometry</subject><subject>Gastric cancer</subject><subject>Helper cells</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Leukemia</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Prognosis</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Rapamycin</subject><subject>Signal transduction</subject><subject>Studies</subject><subject>Surgery</subject><subject>TOR protein</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNo9UMtKAzEUDaJgrS78g4ArF1PzmEwmy1J8FIqC1PWQydxoyrxMpmB3foL-ol9iOhXv5r7OuYd7ELqkZEZj3BgdZpSnTB2hScwqkYRkx2MtE0U4O0VnIWwI4Vmq0gn6XrbGgw5Q4fXP59cb1D14TCU2UNe4ctaCh3ZwenBdixuoYhWx5Q7DRxe6BiLpf9o44zv8_DjHcZoKin3chMG7cjvSXYtf9b432OjWRCHXWlcPfmSvR81wjk6srgNc_OUperm7XS8ektXT_XIxXyWGEsYSa0Rm8lJKnUElSCYqKnMtGOSMQSqBU2Ms00xQoKVVSpR5RljO08pQbXPBp-jqcLf33fsWwlBsuq1vo2TBWK4EE4KwiLo-oOJnIXiwRe9do_2uoKTYO15Ex4vRcf4LdRR3eA</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Liu, Feng</creator><creator>Bu, Zhouyan</creator><creator>Zhao, Feng</creator><creator>Xiao, Daping</creator><general>John Wiley & Sons, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-4422-6389</orcidid></search><sort><creationdate>201801</creationdate><title>Increased T‐helper 17 cell differentiation mediated by exosome‐mediated micro RNA ‐451 redistribution in gastric cancer infiltrated T cells</title><author>Liu, Feng ; Bu, Zhouyan ; Zhao, Feng ; Xiao, Daping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1022-fc56c8b77a6ed5065d178a52e822e47e31ccf2a251e1bf995b8602834dc1af853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>AMP</topic><topic>Apoptosis</topic><topic>Blood</topic><topic>Cell culture</topic><topic>Cell differentiation</topic><topic>Cell growth</topic><topic>Exosomes</topic><topic>Flow cytometry</topic><topic>Gastric cancer</topic><topic>Helper cells</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Leukemia</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Prognosis</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Rapamycin</topic><topic>Signal transduction</topic><topic>Studies</topic><topic>Surgery</topic><topic>TOR protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Feng</creatorcontrib><creatorcontrib>Bu, Zhouyan</creatorcontrib><creatorcontrib>Zhao, Feng</creatorcontrib><creatorcontrib>Xiao, Daping</creatorcontrib><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</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><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Feng</au><au>Bu, Zhouyan</au><au>Zhao, Feng</au><au>Xiao, Daping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased T‐helper 17 cell differentiation mediated by exosome‐mediated micro RNA ‐451 redistribution in gastric cancer infiltrated T cells</atitle><jtitle>Cancer science</jtitle><date>2018-01</date><risdate>2018</risdate><volume>109</volume><issue>1</issue><spage>65</spage><epage>73</epage><pages>65-73</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Micro
RNA
(miR)‐451 is a cell metabolism‐related mi
RNA
that can mediate cell energy‐consuming models by several targets. As miR‐451 can promote mechanistic target of rapamycin (
mTOR
) activity, and increased
mTOR
activity is related to increased differentiation of T‐helper 17 (Th17) cells, we sought to investigate whether miR‐451 can redistribute from cancer cells to infiltrated T cells and enhance the distribution of Th17 cells through
mTOR
. Real‐time
PCR
was used for detecting expression of miR‐451 in gastric cancer, tumor infiltrated T cells and exosomes, and distribution of Th17 was evaluated by both flow cytometry and immunohistochemistry (
IHC
). Immunofluorescence staining was used in monitoring the exosome‐enveloped miR‐451 from cancer cells to T cells with different treatments, and signaling pathway change was analyzed by western blot. miR‐451 decreased significantly in gastric cancer (
GC
) tissues but increased in infiltrated T cells and exosomes; tumor miR‐451 was negatively related to infiltrated T cells and exosome miR‐451. Exosome miR‐451 can not only serve as an indicator for poor prognosis of post‐operation
GC
patients but is also related to increased Th17 distribution in gastric cancer. miR‐451 can redistribute from cancer cells to T cells with low glucose treatment. Decreased 5′
AMP
‐activated protein kinase (
AMPK
) and increased
mTOR
activity was investigated in miR‐451 redistributed T cells and the Th17 polarized differentiation of these T cells were also increased. Exosome miR‐451 derived from tumor tissues can serve as an indicator for poor prognosis and redistribution of miR‐451 from cancer cells to infiltrated T cells in low glucose treatment can enhance Th17 differentiation by enhancing
mTOR
activity.</abstract><cop>Tokyo</cop><pub>John Wiley & Sons, Inc</pub><doi>10.1111/cas.13429</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-4422-6389</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Cancer science, 2018-01, Vol.109 (1), p.65-73 |
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| language | eng |
| recordid | cdi_proquest_journals_2289525502 |
| source | Wiley Journals; DOAJ Directory of Open Access Journals; Wiley-Blackwell Open Access Titles; PubMed Central |
| subjects | AMP Apoptosis Blood Cell culture Cell differentiation Cell growth Exosomes Flow cytometry Gastric cancer Helper cells Immunofluorescence Immunohistochemistry Leukemia Lymphocytes Lymphocytes T Medical prognosis Medical research Metastasis MicroRNAs miRNA Prognosis Protein kinase Proteins Rapamycin Signal transduction Studies Surgery TOR protein |
| title | Increased T‐helper 17 cell differentiation mediated by exosome‐mediated micro RNA ‐451 redistribution in gastric cancer infiltrated T cells |
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