Galectin-1 induces metastasis and epithelial-mesenchymal transition (EMT) in human ovarian cancer cells via activation of the MAPK JNK/p38 signalling pathway
Identifieur interne : 000810 ( Ncbi/Merge ); précédent : 000809; suivant : 000811Galectin-1 induces metastasis and epithelial-mesenchymal transition (EMT) in human ovarian cancer cells via activation of the MAPK JNK/p38 signalling pathway
Auteurs : Jie Zhu [République populaire de Chine] ; Ya Zheng [République populaire de Chine] ; Haiyan Zhang [République populaire de Chine] ; Yanmei Liu [République populaire de Chine] ; Hong Sun [République populaire de Chine] ; Pengnan Zhang [République populaire de Chine]Source :
- American Journal of Translational Research [ 1943-8141 ] ; 2019.
Abstract
Background: It has been reported that Galectin-1 (Gal-1) indicates bad prognosis of patients with ovarian cancer, and Gal-1 overexpression promotes metastasis of ovarian cancer cells. Nevertheless, the underlying mechanisms of the Gal-1-mediated enhancement of metastasis are still unclear. Furthermore, little is known about whether Gal-1 affects epithelial-mesenchymal transition (EMT) in ovarian cancer. Methods: The human SKOV3-ip and SKOV3 cell lines were transfected with Gal-1 siRNAs and LV-Gal-1 lentivirus, respectively. Cell migration and cell invasion abilities were examined by transwell assays. Protein or mRNA levels of Gal-1, p-JNK1/2, t-JNK1/2, p-p38, t-p38 and EMT markers were detected via immunohistochemistry, qRT-PCR and western blot in SKOV3-ip as well as SKOV3 cells. A xenograft tumour model was used in vivo to ascertain whether upregulation of Gal-1 in ovarian cancer cells can enhance metastasis in vivo. Results: In a total of 107 human ovarian cancer tissues, higher Gal-1 expression strongly associated with higher histological grade, more lymph node metastases and more advanced FIGO stage, while lower E-cadherin expression strongly associated with higher histological grade, more lymph node metastases and more advanced FIGO stage. In vitro assays revealed that Gal-1 promoted migration and invasion of ovarian cancer cells, as well as EMT. Additionally, the results showed that Gal-1 enhanced EMT, migration and invasion by activating the MAPK JNK/p38 signalling pathway. Moreover, in vivo bioluminescence imaging revealed that Gal-1 modulated ovarian cancer metastasis in nude mice. Immunochemistry of xenograft tumour tissues confirmed that Gal-1 may modulate metastasis and EMT via the MAPK JNK/p38 signalling pathway. Additionally, treatment of Gal-1 mice with the MAPK JNK/p38 signalling pathway antagonists SB203580 or SP600125 reduced cancer metastasis. Conclusion: Gal-1 enhances metastasis and EMT of ovarian cancer cells via promoting the activation of the MAPK JNK/p38 signalling pathway, suggesting the possibility that Gal-1 is a molecular target to prevent and cure ovarian cancer metastasis.
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PubMed: 31312395
PubMed Central: 6614631
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<front><div type="abstract" xml:lang="en"><p>Background: It has been reported that Galectin-1 (Gal-1) indicates bad prognosis of patients with ovarian cancer, and Gal-1 overexpression promotes metastasis of ovarian cancer cells. Nevertheless, the underlying mechanisms of the Gal-1-mediated enhancement of metastasis are still unclear. Furthermore, little is known about whether Gal-1 affects epithelial-mesenchymal transition (EMT) in ovarian cancer. Methods: The human SKOV3-ip and SKOV3 cell lines were transfected with Gal-1 siRNAs and LV-Gal-1 lentivirus, respectively. Cell migration and cell invasion abilities were examined by transwell assays. Protein or mRNA levels of Gal-1, p-JNK1/2, t-JNK1/2, p-p38, t-p38 and EMT markers were detected via immunohistochemistry, qRT-PCR and western blot in SKOV3-ip as well as SKOV3 cells. A xenograft tumour model was used in vivo to ascertain whether upregulation of Gal-1 in ovarian cancer cells can enhance metastasis in vivo. Results: In a total of 107 human ovarian cancer tissues, higher Gal-1 expression strongly associated with higher histological grade, more lymph node metastases and more advanced FIGO stage, while lower E-cadherin expression strongly associated with higher histological grade, more lymph node metastases and more advanced FIGO stage. In vitro assays revealed that Gal-1 promoted migration and invasion of ovarian cancer cells, as well as EMT. Additionally, the results showed that Gal-1 enhanced EMT, migration and invasion by activating the MAPK JNK/p38 signalling pathway. Moreover, in vivo bioluminescence imaging revealed that Gal-1 modulated ovarian cancer metastasis in nude mice. Immunochemistry of xenograft tumour tissues confirmed that Gal-1 may modulate metastasis and EMT via the MAPK JNK/p38 signalling pathway. Additionally, treatment of Gal-1 mice with the MAPK JNK/p38 signalling pathway antagonists SB203580 or SP600125 reduced cancer metastasis. Conclusion: Gal-1 enhances metastasis and EMT of ovarian cancer cells via promoting the activation of the MAPK JNK/p38 signalling pathway, suggesting the possibility that Gal-1 is a molecular target to prevent and cure ovarian cancer metastasis.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Transl Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Am J Transl Res</journal-id>
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<article-categories><subj-group subj-group-type="heading"><subject>Original Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Galectin-1 induces metastasis and epithelial-mesenchymal transition (EMT) in human ovarian cancer cells via activation of the MAPK JNK/p38 signalling pathway</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Zhu</surname>
<given-names>Jie</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zheng</surname>
<given-names>Ya</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Haiyan</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Liu</surname>
<given-names>Yanmei</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sun</surname>
<given-names>Hong</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
<xref ref-type="author-notes" rid="fn1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Pengnan</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
<xref ref-type="author-notes" rid="fn1">*</xref>
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<aff id="au1"><label>1</label>
<institution>Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University</institution>
<addr-line>Shanghai 200011, China</addr-line>
</aff>
<aff id="au2"><label>2</label>
<institution>Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases</institution>
<addr-line>Shanghai 200011, China</addr-line>
</aff>
</contrib-group>
<author-notes><corresp><bold>Address correspondence to:</bold>
Drs. Pengnan Zhang and Hong Sun, Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, 128 Shenyang Road, Shanghai 200011, China. Tel: +86 21 33189900; Fax: +86 21 33189900; E-mail: <email>sydzpn@163.com</email>
(PNZ); <email>hongsun57@hotmail.com</email>
(HS)</corresp>
<fn id="fn1"><label>*</label>
<p>Equal contributors.</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<pub-date pub-type="epub"><day>15</day>
<month>6</month>
<year>2019</year>
</pub-date>
<volume>11</volume>
<issue>6</issue>
<fpage>3862</fpage>
<lpage>3878</lpage>
<history><date date-type="received"><day>21</day>
<month>4</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>19</day>
<month>5</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>AJTR Copyright © 2019</copyright-statement>
<copyright-year>2019</copyright-year>
</permissions>
<abstract><p>Background: It has been reported that Galectin-1 (Gal-1) indicates bad prognosis of patients with ovarian cancer, and Gal-1 overexpression promotes metastasis of ovarian cancer cells. Nevertheless, the underlying mechanisms of the Gal-1-mediated enhancement of metastasis are still unclear. Furthermore, little is known about whether Gal-1 affects epithelial-mesenchymal transition (EMT) in ovarian cancer. Methods: The human SKOV3-ip and SKOV3 cell lines were transfected with Gal-1 siRNAs and LV-Gal-1 lentivirus, respectively. Cell migration and cell invasion abilities were examined by transwell assays. Protein or mRNA levels of Gal-1, p-JNK1/2, t-JNK1/2, p-p38, t-p38 and EMT markers were detected via immunohistochemistry, qRT-PCR and western blot in SKOV3-ip as well as SKOV3 cells. A xenograft tumour model was used in vivo to ascertain whether upregulation of Gal-1 in ovarian cancer cells can enhance metastasis in vivo. Results: In a total of 107 human ovarian cancer tissues, higher Gal-1 expression strongly associated with higher histological grade, more lymph node metastases and more advanced FIGO stage, while lower E-cadherin expression strongly associated with higher histological grade, more lymph node metastases and more advanced FIGO stage. In vitro assays revealed that Gal-1 promoted migration and invasion of ovarian cancer cells, as well as EMT. Additionally, the results showed that Gal-1 enhanced EMT, migration and invasion by activating the MAPK JNK/p38 signalling pathway. Moreover, in vivo bioluminescence imaging revealed that Gal-1 modulated ovarian cancer metastasis in nude mice. Immunochemistry of xenograft tumour tissues confirmed that Gal-1 may modulate metastasis and EMT via the MAPK JNK/p38 signalling pathway. Additionally, treatment of Gal-1 mice with the MAPK JNK/p38 signalling pathway antagonists SB203580 or SP600125 reduced cancer metastasis. Conclusion: Gal-1 enhances metastasis and EMT of ovarian cancer cells via promoting the activation of the MAPK JNK/p38 signalling pathway, suggesting the possibility that Gal-1 is a molecular target to prevent and cure ovarian cancer metastasis.</p>
</abstract>
<kwd-group><kwd>Galectin-1 (Gal-1)</kwd>
<kwd>ovarian cancer</kwd>
<kwd>epithelial-mesenchymal transition (EMT)</kwd>
<kwd>MAPK JNK/p38 signalling pathway</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhu, Jie" sort="Zhu, Jie" uniqKey="Zhu J" first="Jie" last="Zhu">Jie Zhu</name>
</noRegion>
<name sortKey="Liu, Yanmei" sort="Liu, Yanmei" uniqKey="Liu Y" first="Yanmei" last="Liu">Yanmei Liu</name>
<name sortKey="Liu, Yanmei" sort="Liu, Yanmei" uniqKey="Liu Y" first="Yanmei" last="Liu">Yanmei Liu</name>
<name sortKey="Sun, Hong" sort="Sun, Hong" uniqKey="Sun H" first="Hong" last="Sun">Hong Sun</name>
<name sortKey="Sun, Hong" sort="Sun, Hong" uniqKey="Sun H" first="Hong" last="Sun">Hong Sun</name>
<name sortKey="Zhang, Haiyan" sort="Zhang, Haiyan" uniqKey="Zhang H" first="Haiyan" last="Zhang">Haiyan Zhang</name>
<name sortKey="Zhang, Haiyan" sort="Zhang, Haiyan" uniqKey="Zhang H" first="Haiyan" last="Zhang">Haiyan Zhang</name>
<name sortKey="Zhang, Pengnan" sort="Zhang, Pengnan" uniqKey="Zhang P" first="Pengnan" last="Zhang">Pengnan Zhang</name>
<name sortKey="Zhang, Pengnan" sort="Zhang, Pengnan" uniqKey="Zhang P" first="Pengnan" last="Zhang">Pengnan Zhang</name>
<name sortKey="Zheng, Ya" sort="Zheng, Ya" uniqKey="Zheng Y" first="Ya" last="Zheng">Ya Zheng</name>
<name sortKey="Zheng, Ya" sort="Zheng, Ya" uniqKey="Zheng Y" first="Ya" last="Zheng">Ya Zheng</name>
<name sortKey="Zhu, Jie" sort="Zhu, Jie" uniqKey="Zhu J" first="Jie" last="Zhu">Jie Zhu</name>
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