Cancer-associated fibroblasts endow stem-like qualities to liver cancer cells by modulating autophagy
Identifieur interne : 000442 ( Pmc/Curation ); précédent : 000441; suivant : 000443Cancer-associated fibroblasts endow stem-like qualities to liver cancer cells by modulating autophagy
Auteurs : Zhenxiong Zhao [République populaire de Chine] ; Shuya Bai [République populaire de Chine] ; Ronghua Wang [République populaire de Chine] ; Si Xiong [République populaire de Chine] ; Yawen Li [République populaire de Chine] ; Xiju Wang [République populaire de Chine] ; Wei Chen [République populaire de Chine] ; Bin Cheng [République populaire de Chine]Source :
- Cancer Management and Research [ 1179-1322 ] ; 2019.
Abstract
Both cancer-associated fibroblasts (CAFs) and liver cancer stem cells (LCSCs) play an important part in the tumorigenesis, development and metastasis of hepatocellular carcinoma (HCC). Moreover, the stem-like properties in HCC cells could be promoted by CAFs. However, the mechanism remains largely unknown.
We used conditioned medium (CM) of CAFs to culture Huh7 cells. Stemness of the cells was then examined mainly by sphere formation assay while stemness-associated genes including Nanog, Sox2 and Oct4 were measured by Western blotting. Immunofluorescence staining, Transmission Electron Microscope as well as Western blotting were performed to detect the level of autophagy in Huh7 cells.
Increased level of stemness and autophagy was observed in HCC cells cultured in CAFs-CM compared to the control group. Activation of CAFs-induced autophagic flux could be inhibited by Chloroquine (CQ), which can accumulate LC3-II protein and increase punctate distribution of LC3 localization. Treatment of HCC cells with CQ effectively reversed the CAF-induced stemness, invasion, and metastasis ability in these cells. In vivo, Huh7 cells inoculated together with CAFs developed significantly larger tumors than Huh7 cells injected alone. Moreover, blockage of autophagy in Huh7 cells by CQ greatly reduced the growth of xenografted tumors of Huh7 cells combined with CAFs.
These results reveal that CAFs are capable of promoting stemness and metastasis of HCC cells and blocking autophagy could markedly attenuate the stemness enhanced by CAFs, suggesting that targeting autophagy in HCC could be an effective strategy in HCC treatment.
Url:
DOI: 10.2147/CMAR.S197634
PubMed: 31296998
PubMed Central: 6598753
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<front><div type="abstract" xml:lang="en"><sec id="S2001"><title>Purpose</title>
<p>Both cancer-associated fibroblasts (CAFs) and liver cancer stem cells (LCSCs) play an important part in the tumorigenesis, development and metastasis of hepatocellular carcinoma (HCC). Moreover, the stem-like properties in HCC cells could be promoted by CAFs. However, the mechanism remains largely unknown.</p>
</sec>
<sec id="S2002"><title>Patients and methods</title>
<p>We used conditioned medium (CM) of CAFs to culture Huh7 cells. Stemness of the cells was then examined mainly by sphere formation assay while stemness-associated genes including Nanog, Sox2 and Oct4 were measured by Western blotting. Immunofluorescence staining, Transmission Electron Microscope as well as Western blotting were performed to detect the level of autophagy in Huh7 cells.</p>
</sec>
<sec id="S2003"><title>Results</title>
<p>Increased level of stemness and autophagy was observed in HCC cells cultured in CAFs-CM compared to the control group. Activation of CAFs-induced autophagic flux could be inhibited by Chloroquine (CQ), which can accumulate LC3-II protein and increase punctate distribution of LC3 localization. Treatment of HCC cells with CQ effectively reversed the CAF-induced stemness, invasion, and metastasis ability in these cells. In vivo, Huh7 cells inoculated together with CAFs developed significantly larger tumors than Huh7 cells injected alone. Moreover, blockage of autophagy in Huh7 cells by CQ greatly reduced the growth of xenografted tumors of Huh7 cells combined with CAFs.</p>
</sec>
<sec id="S2004"><title>Conclusion</title>
<p>These results reveal that CAFs are capable of promoting stemness and metastasis of HCC cells and blocking autophagy could markedly attenuate the stemness enhanced by CAFs, suggesting that targeting autophagy in HCC could be an effective strategy in HCC treatment.</p>
</sec>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cancer Manag Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Cancer Manag Res</journal-id>
<journal-id journal-id-type="publisher-id">CMAR</journal-id>
<journal-id journal-id-type="pmc">cancmanres</journal-id>
<journal-title-group><journal-title>Cancer Management and Research</journal-title>
</journal-title-group>
<issn pub-type="epub">1179-1322</issn>
<publisher><publisher-name>Dove</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31296998</article-id>
<article-id pub-id-type="pmc">6598753</article-id>
<article-id pub-id-type="publisher-id">197634</article-id>
<article-id pub-id-type="doi">10.2147/CMAR.S197634</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>Cancer-associated fibroblasts endow stem-like qualities to liver cancer cells by modulating autophagy</article-title>
<alt-title alt-title-type="running-authors">Zhao et al</alt-title>
<alt-title alt-title-type="running-title">Zhao et al</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Zhao</surname>
<given-names>Zhenxiong</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bai</surname>
<given-names>Shuya</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Ronghua</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xiong</surname>
<given-names>Si</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Yawen</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Xiju</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Wei</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cheng</surname>
<given-names>Bin</given-names>
</name>
<xref ref-type="corresp" rid="AN0001"></xref>
<xref ref-type="aff" rid="AFF0001">1</xref>
</contrib>
<aff id="AFF0001"><label>1</label>
<institution>Department of Gastroenterology and Hepatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology</institution>
,<addr-line>Wuhan</addr-line>
<addr-line>430030</addr-line>
,<country>People’s Republic of China</country>
</aff>
</contrib-group>
<author-notes><corresp id="AN0001">Correspondence: Bin Cheng<institution>Department of Gastroenterology and Hepatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology</institution>
, <addr-line>Jiefang Avenue. 1095</addr-line>
, <addr-line>Wuhan</addr-line>
<addr-line>430030</addr-line>
, <country>People’s Republic of China</country>
<phone>Tel +86 278 366 3208</phone>
<fax>Fax +86 278 366 3585</fax>
Email <email xlink:href="b.cheng@tjh.tjmu.edu.cn">b.cheng@tjh.tjmu.edu.cn</email>
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>24</day>
<month>6</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>11</volume>
<fpage>5737</fpage>
<lpage>5744</lpage>
<history><date date-type="received"><day>12</day>
<month>12</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>29</day>
<month>5</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© 2019 Zhao et al.</copyright-statement>
<copyright-year>2019</copyright-year>
<copyright-holder>Zhao et al.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/"><license-p>This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at <ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>
and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</ext-link>
). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (<ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>
).</license-p>
</license>
</permissions>
<abstract><sec id="S2001"><title>Purpose</title>
<p>Both cancer-associated fibroblasts (CAFs) and liver cancer stem cells (LCSCs) play an important part in the tumorigenesis, development and metastasis of hepatocellular carcinoma (HCC). Moreover, the stem-like properties in HCC cells could be promoted by CAFs. However, the mechanism remains largely unknown.</p>
</sec>
<sec id="S2002"><title>Patients and methods</title>
<p>We used conditioned medium (CM) of CAFs to culture Huh7 cells. Stemness of the cells was then examined mainly by sphere formation assay while stemness-associated genes including Nanog, Sox2 and Oct4 were measured by Western blotting. Immunofluorescence staining, Transmission Electron Microscope as well as Western blotting were performed to detect the level of autophagy in Huh7 cells.</p>
</sec>
<sec id="S2003"><title>Results</title>
<p>Increased level of stemness and autophagy was observed in HCC cells cultured in CAFs-CM compared to the control group. Activation of CAFs-induced autophagic flux could be inhibited by Chloroquine (CQ), which can accumulate LC3-II protein and increase punctate distribution of LC3 localization. Treatment of HCC cells with CQ effectively reversed the CAF-induced stemness, invasion, and metastasis ability in these cells. In vivo, Huh7 cells inoculated together with CAFs developed significantly larger tumors than Huh7 cells injected alone. Moreover, blockage of autophagy in Huh7 cells by CQ greatly reduced the growth of xenografted tumors of Huh7 cells combined with CAFs.</p>
</sec>
<sec id="S2004"><title>Conclusion</title>
<p>These results reveal that CAFs are capable of promoting stemness and metastasis of HCC cells and blocking autophagy could markedly attenuate the stemness enhanced by CAFs, suggesting that targeting autophagy in HCC could be an effective strategy in HCC treatment.</p>
</sec>
</abstract>
<kwd-group kwd-group-type="author"><title>Keywords</title>
<kwd>cancer-associated fibroblasts</kwd>
<kwd>stemness</kwd>
<kwd>liver cancer</kwd>
<kwd>autophagy</kwd>
</kwd-group>
<counts><fig-count count="4"></fig-count>
<ref-count count="22"></ref-count>
<page-count count="8"></page-count>
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</front>
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