Ginsenoside Rh1 Prevents Migration and Invasion through Mitochondrial ROS-Mediated Inhibition of STAT3/NF-kappa B Signaling in MDA-MB-231 Cells
Breast cancer (BC) a very common cancer in women worldwide. Triple negative breast cancer (TNBC) has been shown to have a poor prognosis with a high level of tumor metastatic spread. Here, the inhibitory effects of ginsenoside-Rh1 (Rh1) on BC metastasis, and its underlying signaling pathway in TNBC...
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| description | Breast cancer (BC) a very common cancer in women worldwide. Triple negative breast cancer (TNBC) has been shown to have a poor prognosis with a high level of tumor metastatic spread. Here, the inhibitory effects of ginsenoside-Rh1 (Rh1) on BC metastasis, and its underlying signaling pathway in TNBC were investigated. Rh1-treated MDA-MB-231 cells were analyzed for metastasis using a wound healing assay, transwell migration and invasion assay, western blotting, and qRT-PCR. Rh1 treatment significantly inhibited BC metastasis by inhibiting the both protein and mRNA levels of MMP2, MMP9, and VEGF-A. Further, Rh1-mediated inhibitory effect on BC migration was associated with mitochondrial ROS generation. Rh1 treatment significantly eliminated STAT3 phosphorylation and NF-kappa B transactivation to downregulate metastatic factors, such as MMP2, MMP9, and VEGF-A. In addition, Mito-TEMPO treatment reversed Rh1 effects on the activation of STAT3, NF-kappa B, and their transcriptional targets. Rh1 further enhanced the inhibitory effects of STAT3 or NF-kappa B specific inhibitor, stattic or BAY 11-7082 on MMP2, MMP9, and VEGF-A expression, respectively. In summary, our results revealed the potent anticancer effect of Rh1 on TNBC migration and invasion through mtROS-mediated inhibition of STAT3 and NF-kappa B signaling. |
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Triple negative breast cancer (TNBC) has been shown to have a poor prognosis with a high level of tumor metastatic spread. Here, the inhibitory effects of ginsenoside-Rh1 (Rh1) on BC metastasis, and its underlying signaling pathway in TNBC were investigated. Rh1-treated MDA-MB-231 cells were analyzed for metastasis using a wound healing assay, transwell migration and invasion assay, western blotting, and qRT-PCR. Rh1 treatment significantly inhibited BC metastasis by inhibiting the both protein and mRNA levels of MMP2, MMP9, and VEGF-A. Further, Rh1-mediated inhibitory effect on BC migration was associated with mitochondrial ROS generation. Rh1 treatment significantly eliminated STAT3 phosphorylation and NF-kappa B transactivation to downregulate metastatic factors, such as MMP2, MMP9, and VEGF-A. In addition, Mito-TEMPO treatment reversed Rh1 effects on the activation of STAT3, NF-kappa B, and their transcriptional targets. Rh1 further enhanced the inhibitory effects of STAT3 or NF-kappa B specific inhibitor, stattic or BAY 11-7082 on MMP2, MMP9, and VEGF-A expression, respectively. In summary, our results revealed the potent anticancer effect of Rh1 on TNBC migration and invasion through mtROS-mediated inhibition of STAT3 and NF-kappa B signaling.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms221910458</identifier><identifier>PMID: 34638797</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>Angiogenesis ; Apoptosis ; Biochemistry & Molecular Biology ; Breast cancer ; Cell adhesion & migration ; Chemistry ; Chemistry, Multidisciplinary ; Cytokines ; Gelatinase A ; Gelatinase B ; ginsenoside Rh1 ; Inflammation ; Kinases ; Life Sciences & Biomedicine ; Liver cancer ; Metastases ; Metastasis ; Mitochondria ; mitochondrial ROS ; Morphology ; Mutation ; NF-κB ; NF-κB protein ; Phosphorylation ; Physical Sciences ; Protein expression ; Proteins ; Science & Technology ; Signal transduction ; STAT3 ; Stat3 protein ; Transcription ; triple-negative breast cancer cells ; Tumorigenesis ; Vascular endothelial growth factor ; Western blotting ; Wound healing</subject><ispartof>International journal of molecular sciences, 2021-10, Vol.22 (19), p.10458, Article 10458</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Triple negative breast cancer (TNBC) has been shown to have a poor prognosis with a high level of tumor metastatic spread. Here, the inhibitory effects of ginsenoside-Rh1 (Rh1) on BC metastasis, and its underlying signaling pathway in TNBC were investigated. Rh1-treated MDA-MB-231 cells were analyzed for metastasis using a wound healing assay, transwell migration and invasion assay, western blotting, and qRT-PCR. Rh1 treatment significantly inhibited BC metastasis by inhibiting the both protein and mRNA levels of MMP2, MMP9, and VEGF-A. Further, Rh1-mediated inhibitory effect on BC migration was associated with mitochondrial ROS generation. Rh1 treatment significantly eliminated STAT3 phosphorylation and NF-kappa B transactivation to downregulate metastatic factors, such as MMP2, MMP9, and VEGF-A. In addition, Mito-TEMPO treatment reversed Rh1 effects on the activation of STAT3, NF-kappa B, and their transcriptional targets. Rh1 further enhanced the inhibitory effects of STAT3 or NF-kappa B specific inhibitor, stattic or BAY 11-7082 on MMP2, MMP9, and VEGF-A expression, respectively. In summary, our results revealed the potent anticancer effect of Rh1 on TNBC migration and invasion through mtROS-mediated inhibition of STAT3 and NF-kappa B signaling.</description><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Biochemistry & Molecular Biology</subject><subject>Breast cancer</subject><subject>Cell adhesion & migration</subject><subject>Chemistry</subject><subject>Chemistry, Multidisciplinary</subject><subject>Cytokines</subject><subject>Gelatinase A</subject><subject>Gelatinase B</subject><subject>ginsenoside Rh1</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Life Sciences & Biomedicine</subject><subject>Liver cancer</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>mitochondrial ROS</subject><subject>Morphology</subject><subject>Mutation</subject><subject>NF-κB</subject><subject>NF-κB protein</subject><subject>Phosphorylation</subject><subject>Physical Sciences</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Science & Technology</subject><subject>Signal transduction</subject><subject>STAT3</subject><subject>Stat3 protein</subject><subject>Transcription</subject><subject>triple-negative breast cancer cells</subject><subject>Tumorigenesis</subject><subject>Vascular endothelial growth factor</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>DOA</sourceid><recordid>eNqNks1v0zAUwCMEYmNw5G6JCxIK80fijwtSV9iotDK0lnPk2E7iktrFTor4K_iXcZtpopw4-dnv9362n16WvUbwPSECXtrNNmKMBIJFyZ9k56jAOIeQsqd_xWfZixg3EGKCS_E8OyMFJZwJdp79vrEuGuej1Qbcdwh8DWZv3BDB0rZBDtY7IJ0GC7eX8bAZuuDHtkvpwavOOx2s7MH93SpfGm3lYA5sZ2t7LPUNWK1na3L55Tr_Lnc7Ca7AyrZO9ta1wDqw_DjLl1c5JgjMTd_Hl9mzRvbRvHpYL7Jv15_W88_57d3NYj67zVX65pCXnHMiKauJIloYKRCSkDEsa4QwLLThUKgGS13IRmlTpo0WWCBcM1ILWZOLbDF5tZebahfsVoZflZe2Oh740FYyDFb1pipFww6XFKikhcZMSGVgoygXtDGc0eT6MLl2Y701WqX2BdmfSE8zznZV6_cVLyGntEyCtw-C4H-MJg7V1kaV2iGd8WOscMkRx4xQntA3_6AbP4bUz4mCiHCKEpVPlAo-xmCax8cgWB3GpjoZm8S_m_ifpvZNVNY4ZR5rIISspARikSJ4sPP_p-d2OE7R3I9uIH8Ay_nUeg</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>Jin, Yujin</creator><creator>Diem Thi Ngoc Huynh</creator><creator>Myung, Chang-Seon</creator><creator>Heo, Kyung-Sun</creator><general>Mdpi</general><general>MDPI AG</general><general>MDPI</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-6292-2911</orcidid><orcidid>https://orcid.org/0000-0003-2560-1841</orcidid></search><sort><creationdate>20211001</creationdate><title>Ginsenoside Rh1 Prevents Migration and Invasion through Mitochondrial ROS-Mediated Inhibition of STAT3/NF-kappa B Signaling in MDA-MB-231 Cells</title><author>Jin, Yujin ; 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Triple negative breast cancer (TNBC) has been shown to have a poor prognosis with a high level of tumor metastatic spread. Here, the inhibitory effects of ginsenoside-Rh1 (Rh1) on BC metastasis, and its underlying signaling pathway in TNBC were investigated. Rh1-treated MDA-MB-231 cells were analyzed for metastasis using a wound healing assay, transwell migration and invasion assay, western blotting, and qRT-PCR. Rh1 treatment significantly inhibited BC metastasis by inhibiting the both protein and mRNA levels of MMP2, MMP9, and VEGF-A. Further, Rh1-mediated inhibitory effect on BC migration was associated with mitochondrial ROS generation. Rh1 treatment significantly eliminated STAT3 phosphorylation and NF-kappa B transactivation to downregulate metastatic factors, such as MMP2, MMP9, and VEGF-A. In addition, Mito-TEMPO treatment reversed Rh1 effects on the activation of STAT3, NF-kappa B, and their transcriptional targets. Rh1 further enhanced the inhibitory effects of STAT3 or NF-kappa B specific inhibitor, stattic or BAY 11-7082 on MMP2, MMP9, and VEGF-A expression, respectively. In summary, our results revealed the potent anticancer effect of Rh1 on TNBC migration and invasion through mtROS-mediated inhibition of STAT3 and NF-kappa B signaling.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>34638797</pmid><doi>10.3390/ijms221910458</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-6292-2911</orcidid><orcidid>https://orcid.org/0000-0003-2560-1841</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Apoptosis Biochemistry & Molecular Biology Breast cancer Cell adhesion & migration Chemistry Chemistry, Multidisciplinary Cytokines Gelatinase A Gelatinase B ginsenoside Rh1 Inflammation Kinases Life Sciences & Biomedicine Liver cancer Metastases Metastasis Mitochondria mitochondrial ROS Morphology Mutation NF-κB NF-κB protein Phosphorylation Physical Sciences Protein expression Proteins Science & Technology Signal transduction STAT3 Stat3 protein Transcription triple-negative breast cancer cells Tumorigenesis Vascular endothelial growth factor Western blotting Wound healing |
| title | Ginsenoside Rh1 Prevents Migration and Invasion through Mitochondrial ROS-Mediated Inhibition of STAT3/NF-kappa B Signaling in MDA-MB-231 Cells |
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