Matrine suppresses breast cancer metastasis by targeting ITGB1 and inhibiting epithelial-to-mesenchymal transition
Identifieur interne : 000600 ( Pmc/Checkpoint ); précédent : 000599; suivant : 000601Matrine suppresses breast cancer metastasis by targeting ITGB1 and inhibiting epithelial-to-mesenchymal transition
Auteurs : Lili Ren [République populaire de Chine] ; Wenju Mo [République populaire de Chine] ; Linling Wang [République populaire de Chine] ; Xiaojia Wang [République populaire de Chine]Source :
- Experimental and Therapeutic Medicine [ 1792-0981 ] ; 2019.
Abstract
Metastasis can be a fatal step in breast cancer progression. Effective therapies are urgently required due to the limited therapeutic options clinically available. The aim of the present study was to investigate the effect of matrine (MAT), a traditional Chinese medicine, on the proliferation and migration of human breast cancer cells and its underlying mechanisms of action. The proliferation of MDA-MB-231 cells was inhibited and apoptosis was induced following treatment with MAT, as determined by MTT and Annexin-V-FITC/PI assays. Western blot analysis was used to detect the LC-3II/I levels and the results suggested that tumor autophagy is involved in the anti-tumor activity of MAT. To the best of our knowledge, this is the first study to report that MAT inhibits MDA-MB-231 and MCF-7 cell motility, potentially by targeting integrin β1 (ITGB1) and epithelial-to-mesenchymal transition (EMT), as indicated by Transwell® and siRNA interference assays. In conclusion, ITGB1 and EMT are involved in MAT-induced breast carcinoma cell death and the inhibition of metastasis. This may lead to the development of novel compounds for the treatment of breast cancer metastasis.
Url:
DOI: 10.3892/etm.2019.8207
PubMed: 31853313
PubMed Central: 6909565
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Matrine suppresses breast cancer metastasis by targeting ITGB1 and inhibiting epithelial-to-mesenchymal transition</title><author><name sortKey="Ren, Lili" sort="Ren, Lili" uniqKey="Ren L" first="Lili" last="Ren">Lili Ren</name><affiliation wicri:level="1"><nlm:aff id="af1-etm-0-0-8207">Department of Integration of Traditional Chinese and Western Medicine, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Integration of Traditional Chinese and Western Medicine, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022</wicri:regionArea><wicri:noRegion>Zhejiang 310022</wicri:noRegion></affiliation></author><author><name sortKey="Mo, Wenju" sort="Mo, Wenju" uniqKey="Mo W" first="Wenju" last="Mo">Wenju Mo</name><affiliation wicri:level="1"><nlm:aff id="af2-etm-0-0-8207">Department of Breast Tumor Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Breast Tumor Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022</wicri:regionArea><wicri:noRegion>Zhejiang 310022</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Linling" sort="Wang, Linling" uniqKey="Wang L" first="Linling" last="Wang">Linling Wang</name><affiliation wicri:level="1"><nlm:aff id="af3-etm-0-0-8207">College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053</wicri:regionArea><wicri:noRegion>Zhejiang 310053</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Xiaojia" sort="Wang, Xiaojia" uniqKey="Wang X" first="Xiaojia" last="Wang">Xiaojia Wang</name><affiliation wicri:level="1"><nlm:aff id="af4-etm-0-0-8207">Department of Medical Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Medical Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022</wicri:regionArea><wicri:noRegion>Zhejiang 310022</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31853313</idno><idno type="pmc">6909565</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6909565</idno><idno type="RBID">PMC:6909565</idno><idno type="doi">10.3892/etm.2019.8207</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000521</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000521</idno><idno type="wicri:Area/Pmc/Curation">000521</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000521</idno><idno type="wicri:Area/Pmc/Checkpoint">000600</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000600</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Matrine suppresses breast cancer metastasis by targeting ITGB1 and inhibiting epithelial-to-mesenchymal transition</title><author><name sortKey="Ren, Lili" sort="Ren, Lili" uniqKey="Ren L" first="Lili" last="Ren">Lili Ren</name><affiliation wicri:level="1"><nlm:aff id="af1-etm-0-0-8207">Department of Integration of Traditional Chinese and Western Medicine, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Integration of Traditional Chinese and Western Medicine, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022</wicri:regionArea><wicri:noRegion>Zhejiang 310022</wicri:noRegion></affiliation></author><author><name sortKey="Mo, Wenju" sort="Mo, Wenju" uniqKey="Mo W" first="Wenju" last="Mo">Wenju Mo</name><affiliation wicri:level="1"><nlm:aff id="af2-etm-0-0-8207">Department of Breast Tumor Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Breast Tumor Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022</wicri:regionArea><wicri:noRegion>Zhejiang 310022</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Linling" sort="Wang, Linling" uniqKey="Wang L" first="Linling" last="Wang">Linling Wang</name><affiliation wicri:level="1"><nlm:aff id="af3-etm-0-0-8207">College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053</wicri:regionArea><wicri:noRegion>Zhejiang 310053</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Xiaojia" sort="Wang, Xiaojia" uniqKey="Wang X" first="Xiaojia" last="Wang">Xiaojia Wang</name><affiliation wicri:level="1"><nlm:aff id="af4-etm-0-0-8207">Department of Medical Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Medical Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022</wicri:regionArea><wicri:noRegion>Zhejiang 310022</wicri:noRegion></affiliation></author></analytic><series><title level="j">Experimental and Therapeutic Medicine</title><idno type="ISSN">1792-0981</idno><idno type="eISSN">1792-1015</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Metastasis can be a fatal step in breast cancer progression. Effective therapies are urgently required due to the limited therapeutic options clinically available. The aim of the present study was to investigate the effect of matrine (MAT), a traditional Chinese medicine, on the proliferation and migration of human breast cancer cells and its underlying mechanisms of action. The proliferation of MDA-MB-231 cells was inhibited and apoptosis was induced following treatment with MAT, as determined by MTT and Annexin-V-FITC/PI assays. Western blot analysis was used to detect the LC-3II/I levels and the results suggested that tumor autophagy is involved in the anti-tumor activity of MAT. To the best of our knowledge, this is the first study to report that MAT inhibits MDA-MB-231 and MCF-7 cell motility, potentially by targeting integrin β1 (ITGB1) and epithelial-to-mesenchymal transition (EMT), as indicated by Transwell<sup>®</sup> and siRNA interference assays. In conclusion, ITGB1 and EMT are involved in MAT-induced breast carcinoma cell death and the inhibition of metastasis. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Exp Ther Med</journal-id><journal-id journal-id-type="iso-abbrev">Exp Ther Med</journal-id><journal-id journal-id-type="publisher-id">ETM</journal-id><journal-title-group><journal-title>Experimental and Therapeutic Medicine</journal-title></journal-title-group><issn pub-type="ppub">1792-0981</issn><issn pub-type="epub">1792-1015</issn><publisher><publisher-name>D.A. Spandidos</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31853313</article-id><article-id pub-id-type="pmc">6909565</article-id><article-id pub-id-type="doi">10.3892/etm.2019.8207</article-id><article-id pub-id-type="publisher-id">ETM-0-0-8207</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Matrine suppresses breast cancer metastasis by targeting ITGB1 and inhibiting epithelial-to-mesenchymal transition</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ren</surname><given-names>Lili</given-names></name><xref ref-type="aff" rid="af1-etm-0-0-8207">1</xref></contrib><contrib contrib-type="author"><name><surname>Mo</surname><given-names>Wenju</given-names></name><xref ref-type="aff" rid="af2-etm-0-0-8207">2</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Linling</given-names></name><xref ref-type="aff" rid="af3-etm-0-0-8207">3</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Xiaojia</given-names></name><xref ref-type="aff" rid="af4-etm-0-0-8207">4</xref><xref rid="c1-etm-0-0-8207" ref-type="corresp"></xref></contrib></contrib-group><aff id="af1-etm-0-0-8207"><label>1</label>Department of Integration of Traditional Chinese and Western Medicine, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</aff><aff id="af2-etm-0-0-8207"><label>2</label>Department of Breast Tumor Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</aff><aff id="af3-etm-0-0-8207"><label>3</label>College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China</aff><aff id="af4-etm-0-0-8207"><label>4</label>Department of Medical Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China</aff><author-notes><corresp id="c1-etm-0-0-8207"><italic>Correspondence to</italic>: Dr Xiaojia Wang, Department of Medical Oncology, Zhejiang Cancer Hospital, 1 Banshan Road, Gongshu, Hangzhou, Zhejiang 310022, P.R. China, E-mail: <email>wangxj@zjcc.org.cn</email></corresp></author-notes><pub-date pub-type="ppub"><month>1</month><year>2020</year></pub-date><pub-date pub-type="epub"><day>18</day><month>11</month><year>2019</year></pub-date><pub-date pub-type="pmc-release"><day>18</day><month>11</month><year>2019</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>19</volume><issue>1</issue><fpage>367</fpage><lpage>374</lpage><history><date date-type="received"><day>27</day><month>11</month><year>2018</year></date><date date-type="accepted"><day>17</day><month>10</month><year>2019</year></date></history><permissions><copyright-statement>Copyright: © Ren et al.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>This is an open access article distributed under the terms of the <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by-nc-nd/4.0/">Creative Commons Attribution-NonCommercial-NoDerivs License</ext-link>, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.</license-p></license></permissions><abstract><p>Metastasis can be a fatal step in breast cancer progression. Effective therapies are urgently required due to the limited therapeutic options clinically available. The aim of the present study was to investigate the effect of matrine (MAT), a traditional Chinese medicine, on the proliferation and migration of human breast cancer cells and its underlying mechanisms of action. The proliferation of MDA-MB-231 cells was inhibited and apoptosis was induced following treatment with MAT, as determined by MTT and Annexin-V-FITC/PI assays. Western blot analysis was used to detect the LC-3II/I levels and the results suggested that tumor autophagy is involved in the anti-tumor activity of MAT. To the best of our knowledge, this is the first study to report that MAT inhibits MDA-MB-231 and MCF-7 cell motility, potentially by targeting integrin β1 (ITGB1) and epithelial-to-mesenchymal transition (EMT), as indicated by Transwell<sup>®</sup> and siRNA interference assays. In conclusion, ITGB1 and EMT are involved in MAT-induced breast carcinoma cell death and the inhibition of metastasis. This may lead to the development of novel compounds for the treatment of breast cancer metastasis.</p></abstract><kwd-group><kwd>matrine</kwd><kwd>breast cancer</kwd><kwd>integrin β1</kwd><kwd>epithelial- mesenchymal transition</kwd></kwd-group></article-meta></front><floats-group><fig id="f1-etm-0-0-8207" orientation="portrait" position="float"><label>Figure 1.</label><caption><p>MAT inhibits MDA-MB-231 and MCF-7 cell growth by inducing cell apoptosis. Following incubation with various concentrations of MAT (0–4 mg/ml) for 24 and 48 h, (A) MDA-MB-231 and (B) MCF-7 cell proliferation was measured by MTT assay. (C) MDA-MB-231 and (D) MCF-7 cells were treated with or without MAT (2 mg/ml) for 48 h and stained with Annexin V (5 µg/ml)/PI (10 µg/ml) prior to being analyzed by flow cytometry. Cells labeled with Annexin V(−) PI(+) are shown in the Q1 area, cells labeled with Annexin V(+) PI(+) in the Q2 area, cells labeled with Annexin V(−) PI(−) in the Q3 area and cells labeled with Annexin V(+) PI(−) in the Q4 area. *P<0.05, **P<0.01 and ***P<0.001 MAT vs. CTL by one-way analysis of variance followed by Student-Newman-Keuls post hoc test. MAT, matrine; NC, negative control; PI, propidium iodide; MAT, matrine; FITC, fluorescein isothiocyanate; CTL, control.</p></caption><graphic xlink:href="etm-19-01-0367-g00"></graphic></fig><fig id="f2-etm-0-0-8207" orientation="portrait" position="float"><label>Figure 2.</label><caption><p>Effect of autophagy in MAT-reduced cell growth. (A) MDA-MB-231 and (B) MCF-7 cell growth analysis was performed following treatment with MAT (0, 1 and 2 mg/ml) for 24 and 48 h or pre-treatment with CQ (10 µM) for 1 h. Western blot analysis of LC3-II/I level in (C) MDA-MB-231 and (D) MCF-7 cells following treatment with vehicle CTL, MAT, CQ and MAT+CQ for 48 h. *P<0.05, **P<0.01 and ***P<0.001 MAT or MAT+CQ vs. CTL, <sup>#</sup>P<0.05 MAT+CQ vs. MAT by one-way analysis of variance followed by Student-Newman-Keuls post hoc test. MAT, matrine; CQ, chloroquine diphosphate salt; CTL, control.</p></caption><graphic xlink:href="etm-19-01-0367-g01"></graphic></fig><fig id="f3-etm-0-0-8207" orientation="portrait" position="float"><label>Figure 3.</label><caption><p>MAT decreases the migratory capacity of MDA-MB-231 cells potentially by targeting ITGB1. (A) Migration was analyzed in MDA-MB-231 and MCF-7 cells with or without MAT treatment (1 and 2 mg/ml) for 48 h. (B) Reverse Transcription-quantitative PCR and (C) western blot analysis of ITGB1 mRNA and protein levels in MDA-MB-231 and MCF-7 cells following MAT treatment. *P<0.05 and **P<0.01 MAT vs. CTL by one-way ANOVA. The expression of ITGB1 was reduced in (D) MDA-MB-231 and (E) MCF-7 cells transfected with ITGB1 siRNA. β-actin was used as a loading control. (F) In the presence of siRNA targeting ITGB1, Transwell<sup>®</sup> assay was conducted to evaluate MDA-MB-231 and MCF-7 cell migration following transfection. Silencing ITGB1 results in decreased MDA-MB-231 and MCF-7 cell migration. *P<0.05, **P<0.01 and ***P<0.001 MAT vs. NC by one-way ANOVA followed by Student-Newman-Keuls post hoc test. MAT, matrine; ITGB1, integrin β1; ANOVA, analysis of variance; CTL, control; NC, negative control; si, small interfering.</p></caption><graphic xlink:href="etm-19-01-0367-g02"></graphic></fig><fig id="f4-etm-0-0-8207" orientation="portrait" position="float"><label>Figure 4.</label><caption><p>MAT regulates the transition between epithelial and mesenchymal phenotypes in breast cancer cells. Western blot analysis of E-cadherin, N-cadherin and vimentin levels in (A) MDA-MB-231 and (B) MCF-7 cells following MAT treatment (2 mg/ml) for 48 h. **P<0.01 and ***P<0.001 MAT vs. CTL by one-way analysis of variance. MAT, matrine; CTL, control; E, endothelial; N, neural.</p></caption><graphic xlink:href="etm-19-01-0367-g03"></graphic></fig></floats-group></pmc><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Ren, Lili" sort="Ren, Lili" uniqKey="Ren L" first="Lili" last="Ren">Lili Ren</name></noRegion><name sortKey="Mo, Wenju" sort="Mo, Wenju" uniqKey="Mo W" first="Wenju" last="Mo">Wenju Mo</name><name sortKey="Wang, Linling" sort="Wang, Linling" uniqKey="Wang L" first="Linling" last="Wang">Linling Wang</name><name sortKey="Wang, Xiaojia" sort="Wang, Xiaojia" uniqKey="Wang X" first="Xiaojia" last="Wang">Xiaojia Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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