Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy
Fucoidan is a marine‐origin sulfated polysaccharide that has gained attention for its anticancer activities. However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In...
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| Veröffentlicht in: | Phytotherapy research 2021-12, Vol.35 (12), p.6904-6917 |
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| creator | Zhang, Nan Xue, Meilan Wang, Qing Liang, Hui Yang, Jia Pei, Zhongqian Qin, Kunpeng |
| description | Fucoidan is a marine‐origin sulfated polysaccharide that has gained attention for its anticancer activities. However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In the present study, the anticancer potential of fucoidan was revealed in MCF‐7 and MDA‐MB‐231 cells. Additionally, we also studied the chemotherapeutic sensitization of fucoidan by combining chemotherapeutic drugs doxorubicin (ADM) and cisplatin (DDP) with fucoidan on breast cancer cells. In the two kinds of human breast cancer cells, cell viability was determined by 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Apoptosis was examined with flow cytometry. Transfection assay was used to examine autophagy flow. Western blot was used to examine the expressions of related proteins. Results suggested that fucoidan could induce autophagy and might enhance the sensitivity of breast cancer cells to chemotherapeutic drugs. Mechanistically, fucoidan induced autophagy in breast cancer cells by down‐regulating m‐TOR/p70S6K/TFEB pathway. In conclusion, our research revealed that fucoidan could induce autophagy of breast cancer cells by mediating m‐TOR/p70S6K/TFEB pathway, thus inhibiting tumor development. Furthermore, fucoidan might enhance the sensitivity of breast cancer cells to ADM and DDP, and this enhancement was related to autophagy. |
| doi_str_mv | 10.1002/ptr.7303 |
| format | Article |
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However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In the present study, the anticancer potential of fucoidan was revealed in MCF‐7 and MDA‐MB‐231 cells. Additionally, we also studied the chemotherapeutic sensitization of fucoidan by combining chemotherapeutic drugs doxorubicin (ADM) and cisplatin (DDP) with fucoidan on breast cancer cells. In the two kinds of human breast cancer cells, cell viability was determined by 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Apoptosis was examined with flow cytometry. Transfection assay was used to examine autophagy flow. Western blot was used to examine the expressions of related proteins. Results suggested that fucoidan could induce autophagy and might enhance the sensitivity of breast cancer cells to chemotherapeutic drugs. Mechanistically, fucoidan induced autophagy in breast cancer cells by down‐regulating m‐TOR/p70S6K/TFEB pathway. In conclusion, our research revealed that fucoidan could induce autophagy of breast cancer cells by mediating m‐TOR/p70S6K/TFEB pathway, thus inhibiting tumor development. Furthermore, fucoidan might enhance the sensitivity of breast cancer cells to ADM and DDP, and this enhancement was related to autophagy.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.7303</identifier><identifier>PMID: 34687482</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Anticancer properties ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Apoptosis ; Autophagy ; Breast cancer ; Breast Neoplasms - drug therapy ; Cell Line, Tumor ; Cell Proliferation ; Cell viability ; chemosensitivity ; Chemotherapy ; Cisplatin ; Doxorubicin ; Drugs ; Female ; Flow cytometry ; Fucoidan ; Humans ; m‐TOR/p70S6K/TFEB signal pathway ; Phagocytosis ; Polysaccharides ; Polysaccharides - pharmacology ; Polysaccharides - therapeutic use ; Sensitivity enhancement ; Transfection ; Tumors</subject><ispartof>Phytotherapy research, 2021-12, Vol.35 (12), p.6904-6917</ispartof><rights>2021 John Wiley & Sons Ltd.</rights><rights>2021 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3493-a99eb08c23ebf3646edef416620f546950092499cde67b99d97642c45fad77373</citedby><cites>FETCH-LOGICAL-c3493-a99eb08c23ebf3646edef416620f546950092499cde67b99d97642c45fad77373</cites><orcidid>0000-0002-7296-0778</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%2Fptr.7303$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fptr.7303$$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/34687482$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Nan</creatorcontrib><creatorcontrib>Xue, Meilan</creatorcontrib><creatorcontrib>Wang, Qing</creatorcontrib><creatorcontrib>Liang, Hui</creatorcontrib><creatorcontrib>Yang, Jia</creatorcontrib><creatorcontrib>Pei, Zhongqian</creatorcontrib><creatorcontrib>Qin, Kunpeng</creatorcontrib><title>Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy</title><title>Phytotherapy research</title><addtitle>Phytother Res</addtitle><description>Fucoidan is a marine‐origin sulfated polysaccharide that has gained attention for its anticancer activities. However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In the present study, the anticancer potential of fucoidan was revealed in MCF‐7 and MDA‐MB‐231 cells. Additionally, we also studied the chemotherapeutic sensitization of fucoidan by combining chemotherapeutic drugs doxorubicin (ADM) and cisplatin (DDP) with fucoidan on breast cancer cells. In the two kinds of human breast cancer cells, cell viability was determined by 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Apoptosis was examined with flow cytometry. Transfection assay was used to examine autophagy flow. Western blot was used to examine the expressions of related proteins. Results suggested that fucoidan could induce autophagy and might enhance the sensitivity of breast cancer cells to chemotherapeutic drugs. Mechanistically, fucoidan induced autophagy in breast cancer cells by down‐regulating m‐TOR/p70S6K/TFEB pathway. In conclusion, our research revealed that fucoidan could induce autophagy of breast cancer cells by mediating m‐TOR/p70S6K/TFEB pathway, thus inhibiting tumor development. Furthermore, fucoidan might enhance the sensitivity of breast cancer cells to ADM and DDP, and this enhancement was related to autophagy.</description><subject>Anticancer properties</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell viability</subject><subject>chemosensitivity</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Doxorubicin</subject><subject>Drugs</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Fucoidan</subject><subject>Humans</subject><subject>m‐TOR/p70S6K/TFEB signal pathway</subject><subject>Phagocytosis</subject><subject>Polysaccharides</subject><subject>Polysaccharides - pharmacology</subject><subject>Polysaccharides - therapeutic use</subject><subject>Sensitivity enhancement</subject><subject>Transfection</subject><subject>Tumors</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kV9r1jAUh4Mo7nUKfgIJeONNZ_41aS5l6BwMFJngXUjT07cZbVKTdNL7fXBbNxUEr3LCec7DOfwQeknJGSWEvZ1LOlOc8EfoQInWFa0Vf4wORNe0ErT5doKe5XxDCNGMiKfohAvZKNGwA7q7DINvffEx4NjjfnHRd3arA24T2Fyws8FBwg7GMWMbOjzHAqF4O2IIw96ctu8-XAbwCWcIefPd-rLiErEbYIpbJ9l5xe2KExyX0RYfjtguJc6DPa7P0ZPejhlePLyn6OuH99fnH6urTxeX5--uKseF5pXVGlrSOMah7bkUEjroBZWSkb4WUtf7fUJr14FUrdadVlIwJ-redkpxxU_Rm3vvnOL3BXIxk8_7YTZAXLJhdSOUVkKJDX39D3oTlxS27QyTlAmmFBF_hS7FnBP0Zk5-smk1lJg9GbMlY_ZkNvTVg3BpJ-j-gL-j2IDqHvjhR1j_KzKfr7_8Ev4EOWKZWQ</recordid><startdate>202112</startdate><enddate>202112</enddate><creator>Zhang, Nan</creator><creator>Xue, Meilan</creator><creator>Wang, Qing</creator><creator>Liang, Hui</creator><creator>Yang, Jia</creator><creator>Pei, Zhongqian</creator><creator>Qin, Kunpeng</creator><general>John Wiley & Sons, Ltd</general><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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7296-0778</orcidid></search><sort><creationdate>202112</creationdate><title>Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy</title><author>Zhang, Nan ; Xue, Meilan ; Wang, Qing ; Liang, Hui ; Yang, Jia ; Pei, Zhongqian ; Qin, Kunpeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3493-a99eb08c23ebf3646edef416620f546950092499cde67b99d97642c45fad77373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Anticancer properties</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell viability</topic><topic>chemosensitivity</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>Doxorubicin</topic><topic>Drugs</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Fucoidan</topic><topic>Humans</topic><topic>m‐TOR/p70S6K/TFEB signal pathway</topic><topic>Phagocytosis</topic><topic>Polysaccharides</topic><topic>Polysaccharides - pharmacology</topic><topic>Polysaccharides - therapeutic use</topic><topic>Sensitivity enhancement</topic><topic>Transfection</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Nan</creatorcontrib><creatorcontrib>Xue, Meilan</creatorcontrib><creatorcontrib>Wang, Qing</creatorcontrib><creatorcontrib>Liang, Hui</creatorcontrib><creatorcontrib>Yang, Jia</creatorcontrib><creatorcontrib>Pei, Zhongqian</creatorcontrib><creatorcontrib>Qin, Kunpeng</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Nan</au><au>Xue, Meilan</au><au>Wang, Qing</au><au>Liang, Hui</au><au>Yang, Jia</au><au>Pei, Zhongqian</au><au>Qin, Kunpeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother Res</addtitle><date>2021-12</date><risdate>2021</risdate><volume>35</volume><issue>12</issue><spage>6904</spage><epage>6917</epage><pages>6904-6917</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>Fucoidan is a marine‐origin sulfated polysaccharide that has gained attention for its anticancer activities. However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In the present study, the anticancer potential of fucoidan was revealed in MCF‐7 and MDA‐MB‐231 cells. Additionally, we also studied the chemotherapeutic sensitization of fucoidan by combining chemotherapeutic drugs doxorubicin (ADM) and cisplatin (DDP) with fucoidan on breast cancer cells. In the two kinds of human breast cancer cells, cell viability was determined by 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Apoptosis was examined with flow cytometry. Transfection assay was used to examine autophagy flow. Western blot was used to examine the expressions of related proteins. Results suggested that fucoidan could induce autophagy and might enhance the sensitivity of breast cancer cells to chemotherapeutic drugs. Mechanistically, fucoidan induced autophagy in breast cancer cells by down‐regulating m‐TOR/p70S6K/TFEB pathway. In conclusion, our research revealed that fucoidan could induce autophagy of breast cancer cells by mediating m‐TOR/p70S6K/TFEB pathway, thus inhibiting tumor development. Furthermore, fucoidan might enhance the sensitivity of breast cancer cells to ADM and DDP, and this enhancement was related to autophagy.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>34687482</pmid><doi>10.1002/ptr.7303</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-7296-0778</orcidid></addata></record> |
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| subjects | Anticancer properties Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis Autophagy Breast cancer Breast Neoplasms - drug therapy Cell Line, Tumor Cell Proliferation Cell viability chemosensitivity Chemotherapy Cisplatin Doxorubicin Drugs Female Flow cytometry Fucoidan Humans m‐TOR/p70S6K/TFEB signal pathway Phagocytosis Polysaccharides Polysaccharides - pharmacology Polysaccharides - therapeutic use Sensitivity enhancement Transfection Tumors |
| title | Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy |
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