Mitochondrial dynamics regulating chemoresistance in gynecological cancers
Chemoresistance enables cancer cells to evade apoptotic stimuli and leads to poor clinical prognosis. It arises from dysregulation of signaling factors responsible for inducing cell proliferation and death and for modulating the microenvironment. In gynecologic cancers, p53 is a pivotal determinant...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2015-09, Vol.1350 (1), p.1-16 |
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| creator | Kong, Bao Tsuyoshi, Hideaki Orisaka, Makoto Shieh, Dar-Bin Yoshida, Yoshio Tsang, Benjamin K. |
| description | Chemoresistance enables cancer cells to evade apoptotic stimuli and leads to poor clinical prognosis. It arises from dysregulation of signaling factors responsible for inducing cell proliferation and death and for modulating the microenvironment. In gynecologic cancers, p53 is a pivotal determinant of cisplatin sensitivity, while BCL‐2 family members are associated with taxane sensitivity. Mitochondria fusion and fission dynamics are required for many mitochondrial functions and are also involved in mitochondria‐mediated apoptosis, which is closely associated with chemosensitivity. Mitochondrial dynamics are controlled by a number of intracellular proteins, including fusion (Opa1 and mitofusion 1 and 2) and fission proteins (Drp1 and Fis1), which can be proapoptotic or antiapoptotic, depending on the cell types, status, and stimuli from the microenvironment. This paper describes the role of mitochondrial dynamics in the mechanism of chemoresistance and the evidence supporting a significant contribution of a hyperfusion state to chemoresistance in gynecological cancers. Moreover, we discuss our findings showing that enforced fission induces apoptosis of cancer cells and sensitizes them to chemotherapeutic agents. Understanding the regulation of mitochondrial dynamics in chemoresistance may provide insight into new biomarkers that better predict cancer chemosensitivity and may aid the development of effective therapeutic strategies for clinical management of gynecologic cancers. |
| doi_str_mv | 10.1111/nyas.12883 |
| format | Article |
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It arises from dysregulation of signaling factors responsible for inducing cell proliferation and death and for modulating the microenvironment. In gynecologic cancers, p53 is a pivotal determinant of cisplatin sensitivity, while BCL‐2 family members are associated with taxane sensitivity. Mitochondria fusion and fission dynamics are required for many mitochondrial functions and are also involved in mitochondria‐mediated apoptosis, which is closely associated with chemosensitivity. Mitochondrial dynamics are controlled by a number of intracellular proteins, including fusion (Opa1 and mitofusion 1 and 2) and fission proteins (Drp1 and Fis1), which can be proapoptotic or antiapoptotic, depending on the cell types, status, and stimuli from the microenvironment. This paper describes the role of mitochondrial dynamics in the mechanism of chemoresistance and the evidence supporting a significant contribution of a hyperfusion state to chemoresistance in gynecological cancers. Moreover, we discuss our findings showing that enforced fission induces apoptosis of cancer cells and sensitizes them to chemotherapeutic agents. Understanding the regulation of mitochondrial dynamics in chemoresistance may provide insight into new biomarkers that better predict cancer chemosensitivity and may aid the development of effective therapeutic strategies for clinical management of gynecologic cancers.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/nyas.12883</identifier><identifier>PMID: 26375862</identifier><identifier>CODEN: ANYAA9</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Animals ; Antineoplastic Agents - therapeutic use ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Apoptosis ; Apoptosis - drug effects ; cancer ; CDDP ; chemoresistance ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Female ; Genital Neoplasms, Female - drug therapy ; Genital Neoplasms, Female - metabolism ; Genital Neoplasms, Female - pathology ; Genitalia, Female - drug effects ; Genitalia, Female - metabolism ; Genitalia, Female - pathology ; Humans ; Mitochondrial DNA ; mitochondrial dynamics ; Mitochondrial Dynamics - drug effects ; Models, Biological ; Ovarian cancer</subject><ispartof>Annals of the New York Academy of Sciences, 2015-09, Vol.1350 (1), p.1-16</ispartof><rights>2015 New York Academy of Sciences.</rights><rights>2015 The New York Academy of Sciences</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5313-6ccb66a813a40dedd4d2884f47b19b1a0ea5168c7bc5e9fa7bba627c9bf884743</citedby><cites>FETCH-LOGICAL-c5313-6ccb66a813a40dedd4d2884f47b19b1a0ea5168c7bc5e9fa7bba627c9bf884743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnyas.12883$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnyas.12883$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26375862$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kong, Bao</creatorcontrib><creatorcontrib>Tsuyoshi, Hideaki</creatorcontrib><creatorcontrib>Orisaka, Makoto</creatorcontrib><creatorcontrib>Shieh, Dar-Bin</creatorcontrib><creatorcontrib>Yoshida, Yoshio</creatorcontrib><creatorcontrib>Tsang, Benjamin K.</creatorcontrib><title>Mitochondrial dynamics regulating chemoresistance in gynecological cancers</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann. N.Y. Acad. Sci</addtitle><description>Chemoresistance enables cancer cells to evade apoptotic stimuli and leads to poor clinical prognosis. It arises from dysregulation of signaling factors responsible for inducing cell proliferation and death and for modulating the microenvironment. In gynecologic cancers, p53 is a pivotal determinant of cisplatin sensitivity, while BCL‐2 family members are associated with taxane sensitivity. Mitochondria fusion and fission dynamics are required for many mitochondrial functions and are also involved in mitochondria‐mediated apoptosis, which is closely associated with chemosensitivity. Mitochondrial dynamics are controlled by a number of intracellular proteins, including fusion (Opa1 and mitofusion 1 and 2) and fission proteins (Drp1 and Fis1), which can be proapoptotic or antiapoptotic, depending on the cell types, status, and stimuli from the microenvironment. This paper describes the role of mitochondrial dynamics in the mechanism of chemoresistance and the evidence supporting a significant contribution of a hyperfusion state to chemoresistance in gynecological cancers. Moreover, we discuss our findings showing that enforced fission induces apoptosis of cancer cells and sensitizes them to chemotherapeutic agents. Understanding the regulation of mitochondrial dynamics in chemoresistance may provide insight into new biomarkers that better predict cancer chemosensitivity and may aid the development of effective therapeutic strategies for clinical management of gynecologic cancers.</description><subject>Animals</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>cancer</subject><subject>CDDP</subject><subject>chemoresistance</subject><subject>Drug Resistance, Multiple</subject><subject>Drug Resistance, Neoplasm</subject><subject>Female</subject><subject>Genital Neoplasms, Female - drug therapy</subject><subject>Genital Neoplasms, Female - metabolism</subject><subject>Genital Neoplasms, Female - pathology</subject><subject>Genitalia, Female - drug effects</subject><subject>Genitalia, Female - metabolism</subject><subject>Genitalia, Female - pathology</subject><subject>Humans</subject><subject>Mitochondrial DNA</subject><subject>mitochondrial dynamics</subject><subject>Mitochondrial Dynamics - drug effects</subject><subject>Models, Biological</subject><subject>Ovarian cancer</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90E9LwzAYBvAgis4_Fz-AFLyI0Nk0adIepehUdB6cqKeQpmkXbZOZtGi_vZnTHTyYywvh9z68PAAcwmgM_TvTA3djGKcp2gAjSHEWEoLiTTCKIkrDNIvRDth17jWKPMJ0G-zEBNEkJfEI3Nypzoi50aVVvAnKQfNWCRdYWfcN75SuAzGXrbHSKddxLWSgdFAPWgrTmFoJvySW39btg62KN04e_Mw98Hh5Mcuvwtv7yXV-fhuKBEEUEiEKQngKEcdRKcsSl_50XGFawKyAPJI8gSQVtBCJzCpOi4KTmIqsqDyjGO2Bk1Xuwpr3XrqOtcoJ2TRcS9M7BilEGSaIQE-P_9BX01vtr1uqmCQQYerV6UoJa5yzsmILq1puBwYjtmyYLRtm3w17fPQT2RetLNf0t1IP4Ap8qEYO_0Sx6cv5w29ouNrxHcvP9Q63b4xQn8uephM2wflsmj0_sRx9AZNQll0</recordid><startdate>201509</startdate><enddate>201509</enddate><creator>Kong, Bao</creator><creator>Tsuyoshi, Hideaki</creator><creator>Orisaka, Makoto</creator><creator>Shieh, Dar-Bin</creator><creator>Yoshida, Yoshio</creator><creator>Tsang, Benjamin K.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>201509</creationdate><title>Mitochondrial dynamics regulating chemoresistance in gynecological cancers</title><author>Kong, Bao ; Tsuyoshi, Hideaki ; Orisaka, Makoto ; Shieh, Dar-Bin ; Yoshida, Yoshio ; Tsang, Benjamin K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5313-6ccb66a813a40dedd4d2884f47b19b1a0ea5168c7bc5e9fa7bba627c9bf884743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>cancer</topic><topic>CDDP</topic><topic>chemoresistance</topic><topic>Drug Resistance, Multiple</topic><topic>Drug Resistance, Neoplasm</topic><topic>Female</topic><topic>Genital Neoplasms, Female - drug therapy</topic><topic>Genital Neoplasms, Female - metabolism</topic><topic>Genital Neoplasms, Female - pathology</topic><topic>Genitalia, Female - drug effects</topic><topic>Genitalia, Female - metabolism</topic><topic>Genitalia, Female - pathology</topic><topic>Humans</topic><topic>Mitochondrial DNA</topic><topic>mitochondrial dynamics</topic><topic>Mitochondrial Dynamics - drug effects</topic><topic>Models, Biological</topic><topic>Ovarian cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kong, Bao</creatorcontrib><creatorcontrib>Tsuyoshi, Hideaki</creatorcontrib><creatorcontrib>Orisaka, Makoto</creatorcontrib><creatorcontrib>Shieh, Dar-Bin</creatorcontrib><creatorcontrib>Yoshida, Yoshio</creatorcontrib><creatorcontrib>Tsang, Benjamin K.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Environment Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kong, Bao</au><au>Tsuyoshi, Hideaki</au><au>Orisaka, Makoto</au><au>Shieh, Dar-Bin</au><au>Yoshida, Yoshio</au><au>Tsang, Benjamin K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial dynamics regulating chemoresistance in gynecological cancers</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann. N.Y. Acad. Sci</addtitle><date>2015-09</date><risdate>2015</risdate><volume>1350</volume><issue>1</issue><spage>1</spage><epage>16</epage><pages>1-16</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><coden>ANYAA9</coden><abstract>Chemoresistance enables cancer cells to evade apoptotic stimuli and leads to poor clinical prognosis. It arises from dysregulation of signaling factors responsible for inducing cell proliferation and death and for modulating the microenvironment. In gynecologic cancers, p53 is a pivotal determinant of cisplatin sensitivity, while BCL‐2 family members are associated with taxane sensitivity. Mitochondria fusion and fission dynamics are required for many mitochondrial functions and are also involved in mitochondria‐mediated apoptosis, which is closely associated with chemosensitivity. Mitochondrial dynamics are controlled by a number of intracellular proteins, including fusion (Opa1 and mitofusion 1 and 2) and fission proteins (Drp1 and Fis1), which can be proapoptotic or antiapoptotic, depending on the cell types, status, and stimuli from the microenvironment. This paper describes the role of mitochondrial dynamics in the mechanism of chemoresistance and the evidence supporting a significant contribution of a hyperfusion state to chemoresistance in gynecological cancers. Moreover, we discuss our findings showing that enforced fission induces apoptosis of cancer cells and sensitizes them to chemotherapeutic agents. Understanding the regulation of mitochondrial dynamics in chemoresistance may provide insight into new biomarkers that better predict cancer chemosensitivity and may aid the development of effective therapeutic strategies for clinical management of gynecologic cancers.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>26375862</pmid><doi>10.1111/nyas.12883</doi><tpages>16</tpages></addata></record> |
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| subjects | Animals Antineoplastic Agents - therapeutic use Antineoplastic Combined Chemotherapy Protocols - therapeutic use Apoptosis Apoptosis - drug effects cancer CDDP chemoresistance Drug Resistance, Multiple Drug Resistance, Neoplasm Female Genital Neoplasms, Female - drug therapy Genital Neoplasms, Female - metabolism Genital Neoplasms, Female - pathology Genitalia, Female - drug effects Genitalia, Female - metabolism Genitalia, Female - pathology Humans Mitochondrial DNA mitochondrial dynamics Mitochondrial Dynamics - drug effects Models, Biological Ovarian cancer |
| title | Mitochondrial dynamics regulating chemoresistance in gynecological cancers |
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