Synergistic effect of anethole and doxorubicin alleviates cell proliferation, cell cycle arrest, and ER stress and promotes ROS‐mediated apoptosis in triple‐negative breast cancer cells
The heterogeneity and poor prognosis of triple‐negative breast cancer (TNBC) have limited the treatment options and made clinical management challenging. This has nurtured a major effort to discover druggable molecular targets. Currently, chemotherapy is the primary treatment strategy for this disea...
Gespeichert in:
| Veröffentlicht in: | Journal of biochemical and molecular toxicology 2021-12, Vol.35 (12), p.e22928-n/a |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | n/a |
|---|---|
| container_issue | 12 |
| container_start_page | e22928 |
| container_title | Journal of biochemical and molecular toxicology |
| container_volume | 35 |
| creator | Arumugam, Poornima Sampathkumar, Banupriya Perumalsamy, Haribalan Balusamy, Sri Renukadevi Ramesh, Vignesh Sundaravadevel, Sumathi |
| description | The heterogeneity and poor prognosis of triple‐negative breast cancer (TNBC) have limited the treatment options and made clinical management challenging. This has nurtured a major effort to discover druggable molecular targets. Currently, chemotherapy is the primary treatment strategy for this disease. Doxorubicin is the most frequently used chemotherapeutic drug for TNBC and due to the fact that chemotherapeutic drugs have a lot of side effects, we evaluated the synergistic effect of the phytocompound anethole and doxorubicin. The cytotoxic effect of anethole in combination with doxorubicin on MDA‐MB‐231 cells was evaluated by various parameters, including apoptosis, cell cycle analysis, DNA damage, and cell proliferation. Furthermore, mitochondrial membranepotential (MMP), endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS) levels were also evaluated in the cells treated with/without anethole and doxorubicin. Expression of the apoptotic proteins was evaluated by Western blot analysis. Initial evaluation of cytotoxicity of anethole on MDA‐MB‐231 cells demonstrated preferential suppression of cell proliferation and when treated along with doxorubicin it showed enhanced cytotoxicity with a synergistic effect. Cell cycle analysis revealed arrest at different stages of the cell cycle, such as sub G0‐G1, G0‐G1, S, and G2M in various treatment groups and apoptotic cell death was subsequently evident with propidium iodide (PI) staining. The synergistic action of anethole and doxorubicin effectively induced mitochondrial membrane potential loss, which, in turn, led to a burst of ROS production, which eventually produced unfolded protein response by damaging the ER. Synergistic anticancer effect was observed on exposure of MDA‐MB‐231 cells to anethole and doxorubicin in inducing cell death.
Induction of apoptosis by anethole and doxorubicin |
| doi_str_mv | 10.1002/jbt.22928 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2577731383</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2577731383</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3538-40ad246b628abc887eb60a5bc6280ad09a14ff24189a6b12a46a1d960299cb353</originalsourceid><addsrcrecordid>eNp1kctu1TAQhiMEohdY8ALIEhsqNa3txI6zLFW5qVKltqwj25kUH-XEwXYKZ8cj8EK8DE_CJCkskFh5PPP7m_H8WfaC0RNGKT_dmHTCec3Vo2yf0brOaSnZ4yUWuZQV3csOYtxQSkVdiafZXlEKJUql9rOfN7sBwp2LyVkCXQc2Ed8RPUD67HvAoCWt_-bDZJx1A9F9D_dOJ4jEQt-TMfjedRB0cn44XnN2Z-eXIUBMxwvh4prEhNe43PDN1s-E66ubX99_bKGdgS3Rox-Tjy4SbJSCG3vA8gB3CL8HYgLomIjVg4WwdIrPsied7iM8fzgPs09vL27P3-eXV-8-nJ9d5rYQhcpLqlteSiO50sYqVYGRVAtjMYElWmtWdh0vmaq1NIzrUmrW1pLyurYGEYfZ65WLo3-Z8FvN1sV5AtyTn2LDRVVVBStUgdJX_0g3fgoDTtdwid4wVogKVUerygYfY4CuGYPb6rBrGG1mTxv0tFk8Re3LB-JkcFd_lX9MRMHpKvjqetj9n9R8fHO7In8DariwgA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2609911357</pqid></control><display><type>article</type><title>Synergistic effect of anethole and doxorubicin alleviates cell proliferation, cell cycle arrest, and ER stress and promotes ROS‐mediated apoptosis in triple‐negative breast cancer cells</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Arumugam, Poornima ; Sampathkumar, Banupriya ; Perumalsamy, Haribalan ; Balusamy, Sri Renukadevi ; Ramesh, Vignesh ; Sundaravadevel, Sumathi</creator><creatorcontrib>Arumugam, Poornima ; Sampathkumar, Banupriya ; Perumalsamy, Haribalan ; Balusamy, Sri Renukadevi ; Ramesh, Vignesh ; Sundaravadevel, Sumathi</creatorcontrib><description>The heterogeneity and poor prognosis of triple‐negative breast cancer (TNBC) have limited the treatment options and made clinical management challenging. This has nurtured a major effort to discover druggable molecular targets. Currently, chemotherapy is the primary treatment strategy for this disease. Doxorubicin is the most frequently used chemotherapeutic drug for TNBC and due to the fact that chemotherapeutic drugs have a lot of side effects, we evaluated the synergistic effect of the phytocompound anethole and doxorubicin. The cytotoxic effect of anethole in combination with doxorubicin on MDA‐MB‐231 cells was evaluated by various parameters, including apoptosis, cell cycle analysis, DNA damage, and cell proliferation. Furthermore, mitochondrial membranepotential (MMP), endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS) levels were also evaluated in the cells treated with/without anethole and doxorubicin. Expression of the apoptotic proteins was evaluated by Western blot analysis. Initial evaluation of cytotoxicity of anethole on MDA‐MB‐231 cells demonstrated preferential suppression of cell proliferation and when treated along with doxorubicin it showed enhanced cytotoxicity with a synergistic effect. Cell cycle analysis revealed arrest at different stages of the cell cycle, such as sub G0‐G1, G0‐G1, S, and G2M in various treatment groups and apoptotic cell death was subsequently evident with propidium iodide (PI) staining. The synergistic action of anethole and doxorubicin effectively induced mitochondrial membrane potential loss, which, in turn, led to a burst of ROS production, which eventually produced unfolded protein response by damaging the ER. Synergistic anticancer effect was observed on exposure of MDA‐MB‐231 cells to anethole and doxorubicin in inducing cell death.
Induction of apoptosis by anethole and doxorubicin</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.22928</identifier><identifier>PMID: 34585488</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Allylbenzene Derivatives - pharmacology ; Anethole ; Anisoles - pharmacology ; Antibiotics, Antineoplastic - pharmacology ; Anticancer properties ; Apoptosis ; Apoptosis - drug effects ; Breast cancer ; Cell cycle ; Cell Cycle Checkpoints - drug effects ; Cell death ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - drug effects ; Chemotherapy ; Cytotoxicity ; Damage ; DNA damage ; Doxorubicin ; Doxorubicin - pharmacology ; Drug Synergism ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - drug effects ; Female ; Health services ; Heterogeneity ; Humans ; Iodides ; Membrane potential ; Mitochondria ; Propidium iodide ; Protein folding ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; reactive oxygen species and apoptosis ; Side effects ; Synergistic effect ; Toxicity ; Triple Negative Breast Neoplasms - metabolism ; Triple Negative Breast Neoplasms - pathology ; triple‐negative breast cancer</subject><ispartof>Journal of biochemical and molecular toxicology, 2021-12, Vol.35 (12), p.e22928-n/a</ispartof><rights>2021 Wiley Periodicals LLC</rights><rights>2021 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3538-40ad246b628abc887eb60a5bc6280ad09a14ff24189a6b12a46a1d960299cb353</citedby><cites>FETCH-LOGICAL-c3538-40ad246b628abc887eb60a5bc6280ad09a14ff24189a6b12a46a1d960299cb353</cites><orcidid>0000-0002-0041-1913 ; 0000-0002-4689-1940</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbt.22928$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbt.22928$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34585488$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arumugam, Poornima</creatorcontrib><creatorcontrib>Sampathkumar, Banupriya</creatorcontrib><creatorcontrib>Perumalsamy, Haribalan</creatorcontrib><creatorcontrib>Balusamy, Sri Renukadevi</creatorcontrib><creatorcontrib>Ramesh, Vignesh</creatorcontrib><creatorcontrib>Sundaravadevel, Sumathi</creatorcontrib><title>Synergistic effect of anethole and doxorubicin alleviates cell proliferation, cell cycle arrest, and ER stress and promotes ROS‐mediated apoptosis in triple‐negative breast cancer cells</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>The heterogeneity and poor prognosis of triple‐negative breast cancer (TNBC) have limited the treatment options and made clinical management challenging. This has nurtured a major effort to discover druggable molecular targets. Currently, chemotherapy is the primary treatment strategy for this disease. Doxorubicin is the most frequently used chemotherapeutic drug for TNBC and due to the fact that chemotherapeutic drugs have a lot of side effects, we evaluated the synergistic effect of the phytocompound anethole and doxorubicin. The cytotoxic effect of anethole in combination with doxorubicin on MDA‐MB‐231 cells was evaluated by various parameters, including apoptosis, cell cycle analysis, DNA damage, and cell proliferation. Furthermore, mitochondrial membranepotential (MMP), endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS) levels were also evaluated in the cells treated with/without anethole and doxorubicin. Expression of the apoptotic proteins was evaluated by Western blot analysis. Initial evaluation of cytotoxicity of anethole on MDA‐MB‐231 cells demonstrated preferential suppression of cell proliferation and when treated along with doxorubicin it showed enhanced cytotoxicity with a synergistic effect. Cell cycle analysis revealed arrest at different stages of the cell cycle, such as sub G0‐G1, G0‐G1, S, and G2M in various treatment groups and apoptotic cell death was subsequently evident with propidium iodide (PI) staining. The synergistic action of anethole and doxorubicin effectively induced mitochondrial membrane potential loss, which, in turn, led to a burst of ROS production, which eventually produced unfolded protein response by damaging the ER. Synergistic anticancer effect was observed on exposure of MDA‐MB‐231 cells to anethole and doxorubicin in inducing cell death.
Induction of apoptosis by anethole and doxorubicin</description><subject>Allylbenzene Derivatives - pharmacology</subject><subject>Anethole</subject><subject>Anisoles - pharmacology</subject><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Anticancer properties</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Breast cancer</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Damage</subject><subject>DNA damage</subject><subject>Doxorubicin</subject><subject>Doxorubicin - pharmacology</subject><subject>Drug Synergism</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Female</subject><subject>Health services</subject><subject>Heterogeneity</subject><subject>Humans</subject><subject>Iodides</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Propidium iodide</subject><subject>Protein folding</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>reactive oxygen species and apoptosis</subject><subject>Side effects</subject><subject>Synergistic effect</subject><subject>Toxicity</subject><subject>Triple Negative Breast Neoplasms - metabolism</subject><subject>Triple Negative Breast Neoplasms - pathology</subject><subject>triple‐negative breast cancer</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctu1TAQhiMEohdY8ALIEhsqNa3txI6zLFW5qVKltqwj25kUH-XEwXYKZ8cj8EK8DE_CJCkskFh5PPP7m_H8WfaC0RNGKT_dmHTCec3Vo2yf0brOaSnZ4yUWuZQV3csOYtxQSkVdiafZXlEKJUql9rOfN7sBwp2LyVkCXQc2Ed8RPUD67HvAoCWt_-bDZJx1A9F9D_dOJ4jEQt-TMfjedRB0cn44XnN2Z-eXIUBMxwvh4prEhNe43PDN1s-E66ubX99_bKGdgS3Rox-Tjy4SbJSCG3vA8gB3CL8HYgLomIjVg4WwdIrPsied7iM8fzgPs09vL27P3-eXV-8-nJ9d5rYQhcpLqlteSiO50sYqVYGRVAtjMYElWmtWdh0vmaq1NIzrUmrW1pLyurYGEYfZ65WLo3-Z8FvN1sV5AtyTn2LDRVVVBStUgdJX_0g3fgoDTtdwid4wVogKVUerygYfY4CuGYPb6rBrGG1mTxv0tFk8Re3LB-JkcFd_lX9MRMHpKvjqetj9n9R8fHO7In8DariwgA</recordid><startdate>202112</startdate><enddate>202112</enddate><creator>Arumugam, Poornima</creator><creator>Sampathkumar, Banupriya</creator><creator>Perumalsamy, Haribalan</creator><creator>Balusamy, Sri Renukadevi</creator><creator>Ramesh, Vignesh</creator><creator>Sundaravadevel, Sumathi</creator><general>Wiley Subscription Services, Inc</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>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0041-1913</orcidid><orcidid>https://orcid.org/0000-0002-4689-1940</orcidid></search><sort><creationdate>202112</creationdate><title>Synergistic effect of anethole and doxorubicin alleviates cell proliferation, cell cycle arrest, and ER stress and promotes ROS‐mediated apoptosis in triple‐negative breast cancer cells</title><author>Arumugam, Poornima ; Sampathkumar, Banupriya ; Perumalsamy, Haribalan ; Balusamy, Sri Renukadevi ; Ramesh, Vignesh ; Sundaravadevel, Sumathi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3538-40ad246b628abc887eb60a5bc6280ad09a14ff24189a6b12a46a1d960299cb353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Allylbenzene Derivatives - pharmacology</topic><topic>Anethole</topic><topic>Anisoles - pharmacology</topic><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Anticancer properties</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Breast cancer</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy</topic><topic>Cytotoxicity</topic><topic>Damage</topic><topic>DNA damage</topic><topic>Doxorubicin</topic><topic>Doxorubicin - pharmacology</topic><topic>Drug Synergism</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Female</topic><topic>Health services</topic><topic>Heterogeneity</topic><topic>Humans</topic><topic>Iodides</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Propidium iodide</topic><topic>Protein folding</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>reactive oxygen species and apoptosis</topic><topic>Side effects</topic><topic>Synergistic effect</topic><topic>Toxicity</topic><topic>Triple Negative Breast Neoplasms - metabolism</topic><topic>Triple Negative Breast Neoplasms - pathology</topic><topic>triple‐negative breast cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arumugam, Poornima</creatorcontrib><creatorcontrib>Sampathkumar, Banupriya</creatorcontrib><creatorcontrib>Perumalsamy, Haribalan</creatorcontrib><creatorcontrib>Balusamy, Sri Renukadevi</creatorcontrib><creatorcontrib>Ramesh, Vignesh</creatorcontrib><creatorcontrib>Sundaravadevel, Sumathi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arumugam, Poornima</au><au>Sampathkumar, Banupriya</au><au>Perumalsamy, Haribalan</au><au>Balusamy, Sri Renukadevi</au><au>Ramesh, Vignesh</au><au>Sundaravadevel, Sumathi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synergistic effect of anethole and doxorubicin alleviates cell proliferation, cell cycle arrest, and ER stress and promotes ROS‐mediated apoptosis in triple‐negative breast cancer cells</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2021-12</date><risdate>2021</risdate><volume>35</volume><issue>12</issue><spage>e22928</spage><epage>n/a</epage><pages>e22928-n/a</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>The heterogeneity and poor prognosis of triple‐negative breast cancer (TNBC) have limited the treatment options and made clinical management challenging. This has nurtured a major effort to discover druggable molecular targets. Currently, chemotherapy is the primary treatment strategy for this disease. Doxorubicin is the most frequently used chemotherapeutic drug for TNBC and due to the fact that chemotherapeutic drugs have a lot of side effects, we evaluated the synergistic effect of the phytocompound anethole and doxorubicin. The cytotoxic effect of anethole in combination with doxorubicin on MDA‐MB‐231 cells was evaluated by various parameters, including apoptosis, cell cycle analysis, DNA damage, and cell proliferation. Furthermore, mitochondrial membranepotential (MMP), endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS) levels were also evaluated in the cells treated with/without anethole and doxorubicin. Expression of the apoptotic proteins was evaluated by Western blot analysis. Initial evaluation of cytotoxicity of anethole on MDA‐MB‐231 cells demonstrated preferential suppression of cell proliferation and when treated along with doxorubicin it showed enhanced cytotoxicity with a synergistic effect. Cell cycle analysis revealed arrest at different stages of the cell cycle, such as sub G0‐G1, G0‐G1, S, and G2M in various treatment groups and apoptotic cell death was subsequently evident with propidium iodide (PI) staining. The synergistic action of anethole and doxorubicin effectively induced mitochondrial membrane potential loss, which, in turn, led to a burst of ROS production, which eventually produced unfolded protein response by damaging the ER. Synergistic anticancer effect was observed on exposure of MDA‐MB‐231 cells to anethole and doxorubicin in inducing cell death.
Induction of apoptosis by anethole and doxorubicin</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>34585488</pmid><doi>10.1002/jbt.22928</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-0041-1913</orcidid><orcidid>https://orcid.org/0000-0002-4689-1940</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1095-6670 |
| ispartof | Journal of biochemical and molecular toxicology, 2021-12, Vol.35 (12), p.e22928-n/a |
| issn | 1095-6670 1099-0461 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2577731383 |
| source | MEDLINE; Access via Wiley Online Library |
| subjects | Allylbenzene Derivatives - pharmacology Anethole Anisoles - pharmacology Antibiotics, Antineoplastic - pharmacology Anticancer properties Apoptosis Apoptosis - drug effects Breast cancer Cell cycle Cell Cycle Checkpoints - drug effects Cell death Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Chemotherapy Cytotoxicity Damage DNA damage Doxorubicin Doxorubicin - pharmacology Drug Synergism Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects Female Health services Heterogeneity Humans Iodides Membrane potential Mitochondria Propidium iodide Protein folding Proteins Reactive oxygen species Reactive Oxygen Species - metabolism reactive oxygen species and apoptosis Side effects Synergistic effect Toxicity Triple Negative Breast Neoplasms - metabolism Triple Negative Breast Neoplasms - pathology triple‐negative breast cancer |
| title | Synergistic effect of anethole and doxorubicin alleviates cell proliferation, cell cycle arrest, and ER stress and promotes ROS‐mediated apoptosis in triple‐negative breast cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T16%3A25%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Synergistic%20effect%20of%20anethole%20and%20doxorubicin%20alleviates%20cell%20proliferation,%20cell%20cycle%20arrest,%20and%20ER%20stress%20and%20promotes%20ROS%E2%80%90mediated%20apoptosis%20in%20triple%E2%80%90negative%20breast%20cancer%20cells&rft.jtitle=Journal%20of%20biochemical%20and%20molecular%20toxicology&rft.au=Arumugam,%20Poornima&rft.date=2021-12&rft.volume=35&rft.issue=12&rft.spage=e22928&rft.epage=n/a&rft.pages=e22928-n/a&rft.issn=1095-6670&rft.eissn=1099-0461&rft_id=info:doi/10.1002/jbt.22928&rft_dat=%3Cproquest_cross%3E2577731383%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2609911357&rft_id=info:pmid/34585488&rfr_iscdi=true |