Amorphophalli Rhizoma inhibits breast cancer growth, proliferation, migration, and invasion via the PI3K/AKT pathway
Amorphophalli Rhizoma (APR) is widely used as an adjuvant treatment for advanced and metastatic triple-negative breast cancer (TNBC), but its effects, potential active ingredients, and mechanism of action on estrogen receptor-positive (ER+) and human epidermal growth factor receptor-positive (HER2+)...
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| Veröffentlicht in: | Journal of ethnopharmacology 2022-03, Vol.286, p.114926-114926, Article 114926 |
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| container_title | Journal of ethnopharmacology |
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| creator | Li, Hailong Chen, Mingcang Yang, Zimei Xu, Chuchu Yu, Qinghong Song, Jiaqing Wang, Mengqian Gao, Xiufei |
| description | Amorphophalli Rhizoma (APR) is widely used as an adjuvant treatment for advanced and metastatic triple-negative breast cancer (TNBC), but its effects, potential active ingredients, and mechanism of action on estrogen receptor-positive (ER+) and human epidermal growth factor receptor-positive (HER2+) breast cancer cells were not reported.
The present study investigated the effects and mechanism of APR on ER+ and HER2+ breast cancer cells.
Rotary evaporation was used to prepare different extracts of APR. Cell activity was assessed using the cell counting kit-8 (CCK-8) method. Wound healing assays were used to assess cell migration, and a cell invasion assay was performed using a Transwell chamber with Matrigel matrix. A xenograft model was used to analyze the inhibitory effects of APR on tumor growth. Bioinformatics analyses were used to explore the potential mechanism of APR in breast cancer. RT–qPCR and Western blotting were performed to reveal the molecular mechanism.
The ethyl acetate extract of APR showed the strongest tumor inhibitory effect on ER+ and HER2+ breast cancer cells compared to petroleum ether or N-butanol extracts. APR inhibited ER+ and HER2+ breast cancer cell growth, proliferation, migration, and invasion via the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.
APR had a significant inhibitory effect on ER+ and HER2+ breast cancer cells via the PI3K/AKT signaling pathway. Therefore, APR may be useful for preventing ER+ and HER2+ breast tumor growth, proliferation, migration, and invasion.
[Display omitted]
•APR inhibited cell growth, proliferation, migration, and invasion in ER + breast cancer cells.•APR inhibited cell growth, proliferation, migration, and invasion in HER2+ breast cancer cells.•APR activated the PI3K/AKT signaling pathway.•Different extracts have different cytotoxicity to different types of breast cancer cells.•Different cytotoxicity plays a key role in the accurate treatment of breast cancer. |
| doi_str_mv | 10.1016/j.jep.2021.114926 |
| format | Article |
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The present study investigated the effects and mechanism of APR on ER+ and HER2+ breast cancer cells.
Rotary evaporation was used to prepare different extracts of APR. Cell activity was assessed using the cell counting kit-8 (CCK-8) method. Wound healing assays were used to assess cell migration, and a cell invasion assay was performed using a Transwell chamber with Matrigel matrix. A xenograft model was used to analyze the inhibitory effects of APR on tumor growth. Bioinformatics analyses were used to explore the potential mechanism of APR in breast cancer. RT–qPCR and Western blotting were performed to reveal the molecular mechanism.
The ethyl acetate extract of APR showed the strongest tumor inhibitory effect on ER+ and HER2+ breast cancer cells compared to petroleum ether or N-butanol extracts. APR inhibited ER+ and HER2+ breast cancer cell growth, proliferation, migration, and invasion via the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.
APR had a significant inhibitory effect on ER+ and HER2+ breast cancer cells via the PI3K/AKT signaling pathway. Therefore, APR may be useful for preventing ER+ and HER2+ breast tumor growth, proliferation, migration, and invasion.
[Display omitted]
•APR inhibited cell growth, proliferation, migration, and invasion in ER + breast cancer cells.•APR inhibited cell growth, proliferation, migration, and invasion in HER2+ breast cancer cells.•APR activated the PI3K/AKT signaling pathway.•Different extracts have different cytotoxicity to different types of breast cancer cells.•Different cytotoxicity plays a key role in the accurate treatment of breast cancer.</description><identifier>ISSN: 0378-8741</identifier><identifier>EISSN: 1872-7573</identifier><identifier>DOI: 10.1016/j.jep.2021.114926</identifier><identifier>PMID: 34929308</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Amorphophalli Rhizoma ; Amorphophallus - chemistry ; Animals ; Antineoplastic Agents, Phytogenic - isolation & purification ; Antineoplastic Agents, Phytogenic - pharmacology ; Breast Neoplasms - drug therapy ; Breast Neoplasms - pathology ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; ER+ breast cancer ; Female ; HER2+ breast cancer ; Humans ; MCF-7 Cells ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Invasiveness - prevention & control ; Phosphatidylinositol 3-Kinase - metabolism ; PI3K/AKT pathway ; Plant Extracts - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Receptor, ErbB-2 - metabolism ; Rhizome ; Xenograft Model Antitumor Assays</subject><ispartof>Journal of ethnopharmacology, 2022-03, Vol.286, p.114926-114926, Article 114926</ispartof><rights>2021</rights><rights>Copyright © 2021. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c353t-e3a09e29bafdd769255e43a784c8680f8561877b76c4130582f50cb1b2cb70d93</citedby><cites>FETCH-LOGICAL-c353t-e3a09e29bafdd769255e43a784c8680f8561877b76c4130582f50cb1b2cb70d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378874121011569$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34929308$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Hailong</creatorcontrib><creatorcontrib>Chen, Mingcang</creatorcontrib><creatorcontrib>Yang, Zimei</creatorcontrib><creatorcontrib>Xu, Chuchu</creatorcontrib><creatorcontrib>Yu, Qinghong</creatorcontrib><creatorcontrib>Song, Jiaqing</creatorcontrib><creatorcontrib>Wang, Mengqian</creatorcontrib><creatorcontrib>Gao, Xiufei</creatorcontrib><title>Amorphophalli Rhizoma inhibits breast cancer growth, proliferation, migration, and invasion via the PI3K/AKT pathway</title><title>Journal of ethnopharmacology</title><addtitle>J Ethnopharmacol</addtitle><description>Amorphophalli Rhizoma (APR) is widely used as an adjuvant treatment for advanced and metastatic triple-negative breast cancer (TNBC), but its effects, potential active ingredients, and mechanism of action on estrogen receptor-positive (ER+) and human epidermal growth factor receptor-positive (HER2+) breast cancer cells were not reported.
The present study investigated the effects and mechanism of APR on ER+ and HER2+ breast cancer cells.
Rotary evaporation was used to prepare different extracts of APR. Cell activity was assessed using the cell counting kit-8 (CCK-8) method. Wound healing assays were used to assess cell migration, and a cell invasion assay was performed using a Transwell chamber with Matrigel matrix. A xenograft model was used to analyze the inhibitory effects of APR on tumor growth. Bioinformatics analyses were used to explore the potential mechanism of APR in breast cancer. RT–qPCR and Western blotting were performed to reveal the molecular mechanism.
The ethyl acetate extract of APR showed the strongest tumor inhibitory effect on ER+ and HER2+ breast cancer cells compared to petroleum ether or N-butanol extracts. APR inhibited ER+ and HER2+ breast cancer cell growth, proliferation, migration, and invasion via the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.
APR had a significant inhibitory effect on ER+ and HER2+ breast cancer cells via the PI3K/AKT signaling pathway. Therefore, APR may be useful for preventing ER+ and HER2+ breast tumor growth, proliferation, migration, and invasion.
[Display omitted]
•APR inhibited cell growth, proliferation, migration, and invasion in ER + breast cancer cells.•APR inhibited cell growth, proliferation, migration, and invasion in HER2+ breast cancer cells.•APR activated the PI3K/AKT signaling pathway.•Different extracts have different cytotoxicity to different types of breast cancer cells.•Different cytotoxicity plays a key role in the accurate treatment of breast cancer.</description><subject>Amorphophalli Rhizoma</subject><subject>Amorphophallus - chemistry</subject><subject>Animals</subject><subject>Antineoplastic Agents, Phytogenic - isolation & purification</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>ER+ breast cancer</subject><subject>Female</subject><subject>HER2+ breast cancer</subject><subject>Humans</subject><subject>MCF-7 Cells</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Neoplasm Invasiveness - prevention & control</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>PI3K/AKT pathway</subject><subject>Plant Extracts - pharmacology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Rhizome</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0378-8741</issn><issn>1872-7573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1L7DAUhoMoOn78ADeSpQs75qNtUlwNcq-KgiK6Dml6ajO0TU0yI_rrjYy6dJUTeN6Xcx6EjimZU0LL8-V8CdOcEUbnlOYVK7fQjErBMlEIvo1mhAuZSZHTPbQfwpIQImhOdtEeT3DFiZyhuBicnzo3dbrvLX7s7IcbNLZjZ2sbA6496BCx0aMBj1-8e4vdGZ68620LXkfrxjM82JefUY9NCq91SD-8thrHDvDDDb89X9w-4UnH7k2_H6KdVvcBjr7fA_T8_9_T5XV2d391c7m4ywwveMyAa1IBq2rdNo0oK1YUkHMtZG5kKUkrizJdK2pRmpxyUkjWFsTUtGamFqSp-AE63fSmfV9XEKIabDDQ93oEtwqKlZTxikmZJ5RuUONdCB5aNXk7aP-uKFFfstVSJdnqS7bayE6Zk-_6VT1A85v4sZuAiw0A6ci1Ba-CsZBMNtaDiapx9o_6T4kTj5o</recordid><startdate>20220325</startdate><enddate>20220325</enddate><creator>Li, Hailong</creator><creator>Chen, Mingcang</creator><creator>Yang, Zimei</creator><creator>Xu, Chuchu</creator><creator>Yu, Qinghong</creator><creator>Song, Jiaqing</creator><creator>Wang, Mengqian</creator><creator>Gao, Xiufei</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20220325</creationdate><title>Amorphophalli Rhizoma inhibits breast cancer growth, proliferation, migration, and invasion via the PI3K/AKT pathway</title><author>Li, Hailong ; Chen, Mingcang ; Yang, Zimei ; Xu, Chuchu ; Yu, Qinghong ; Song, Jiaqing ; Wang, Mengqian ; Gao, Xiufei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c353t-e3a09e29bafdd769255e43a784c8680f8561877b76c4130582f50cb1b2cb70d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Amorphophalli Rhizoma</topic><topic>Amorphophallus - chemistry</topic><topic>Animals</topic><topic>Antineoplastic Agents, Phytogenic - isolation & purification</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>ER+ breast cancer</topic><topic>Female</topic><topic>HER2+ breast cancer</topic><topic>Humans</topic><topic>MCF-7 Cells</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Neoplasm Invasiveness - prevention & control</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>PI3K/AKT pathway</topic><topic>Plant Extracts - pharmacology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Rhizome</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Hailong</creatorcontrib><creatorcontrib>Chen, Mingcang</creatorcontrib><creatorcontrib>Yang, Zimei</creatorcontrib><creatorcontrib>Xu, Chuchu</creatorcontrib><creatorcontrib>Yu, Qinghong</creatorcontrib><creatorcontrib>Song, Jiaqing</creatorcontrib><creatorcontrib>Wang, Mengqian</creatorcontrib><creatorcontrib>Gao, Xiufei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of ethnopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Hailong</au><au>Chen, Mingcang</au><au>Yang, Zimei</au><au>Xu, Chuchu</au><au>Yu, Qinghong</au><au>Song, Jiaqing</au><au>Wang, Mengqian</au><au>Gao, Xiufei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amorphophalli Rhizoma inhibits breast cancer growth, proliferation, migration, and invasion via the PI3K/AKT pathway</atitle><jtitle>Journal of ethnopharmacology</jtitle><addtitle>J Ethnopharmacol</addtitle><date>2022-03-25</date><risdate>2022</risdate><volume>286</volume><spage>114926</spage><epage>114926</epage><pages>114926-114926</pages><artnum>114926</artnum><issn>0378-8741</issn><eissn>1872-7573</eissn><abstract>Amorphophalli Rhizoma (APR) is widely used as an adjuvant treatment for advanced and metastatic triple-negative breast cancer (TNBC), but its effects, potential active ingredients, and mechanism of action on estrogen receptor-positive (ER+) and human epidermal growth factor receptor-positive (HER2+) breast cancer cells were not reported.
The present study investigated the effects and mechanism of APR on ER+ and HER2+ breast cancer cells.
Rotary evaporation was used to prepare different extracts of APR. Cell activity was assessed using the cell counting kit-8 (CCK-8) method. Wound healing assays were used to assess cell migration, and a cell invasion assay was performed using a Transwell chamber with Matrigel matrix. A xenograft model was used to analyze the inhibitory effects of APR on tumor growth. Bioinformatics analyses were used to explore the potential mechanism of APR in breast cancer. RT–qPCR and Western blotting were performed to reveal the molecular mechanism.
The ethyl acetate extract of APR showed the strongest tumor inhibitory effect on ER+ and HER2+ breast cancer cells compared to petroleum ether or N-butanol extracts. APR inhibited ER+ and HER2+ breast cancer cell growth, proliferation, migration, and invasion via the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.
APR had a significant inhibitory effect on ER+ and HER2+ breast cancer cells via the PI3K/AKT signaling pathway. Therefore, APR may be useful for preventing ER+ and HER2+ breast tumor growth, proliferation, migration, and invasion.
[Display omitted]
•APR inhibited cell growth, proliferation, migration, and invasion in ER + breast cancer cells.•APR inhibited cell growth, proliferation, migration, and invasion in HER2+ breast cancer cells.•APR activated the PI3K/AKT signaling pathway.•Different extracts have different cytotoxicity to different types of breast cancer cells.•Different cytotoxicity plays a key role in the accurate treatment of breast cancer.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>34929308</pmid><doi>10.1016/j.jep.2021.114926</doi><tpages>1</tpages></addata></record> |
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| subjects | Amorphophalli Rhizoma Amorphophallus - chemistry Animals Antineoplastic Agents, Phytogenic - isolation & purification Antineoplastic Agents, Phytogenic - pharmacology Breast Neoplasms - drug therapy Breast Neoplasms - pathology Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects ER+ breast cancer Female HER2+ breast cancer Humans MCF-7 Cells Mice Mice, Inbred BALB C Mice, Nude Neoplasm Invasiveness - prevention & control Phosphatidylinositol 3-Kinase - metabolism PI3K/AKT pathway Plant Extracts - pharmacology Proto-Oncogene Proteins c-akt - metabolism Receptor, ErbB-2 - metabolism Rhizome Xenograft Model Antitumor Assays |
| title | Amorphophalli Rhizoma inhibits breast cancer growth, proliferation, migration, and invasion via the PI3K/AKT pathway |
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