Sodium butyrate induces growth arrest and senescence‐like phenotypes in gynecologic cancer cells
We demonstrated here the growth‐suppressing effects of sodium butyrate (NaB) on human endometrial and ovarian cancer cells. The arrest of cells at the G1 checkpoint accounted for this effect. NaB‐mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unpho...
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| Veröffentlicht in: | International journal of cancer 2001-10, Vol.94 (2), p.257-267 |
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| creator | Terao, Yasuhisa Nishida, Jun‐ichi Horiuchi, Shinji Rong, Fengnian Ueoka, Yousuke Matsuda, Takao Kato, Hidenori Furugen, Yoshiaki Yoshida, Koyo Kato, Kiyoko Wake, Norio |
| description | We demonstrated here the growth‐suppressing effects of sodium butyrate (NaB) on human endometrial and ovarian cancer cells. The arrest of cells at the G1 checkpoint accounted for this effect. NaB‐mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation. To demonstrate the role of pRb regulation by p21, we measured the sensitivity to NaB of cervical cancer cells in which pRb had been inactivated by HPV E7. The cervical cancer cells displayed a sensitivity in NaB‐mediated G2/M arrest in addition to their sensitivity in G0/G1 arrest. Arrest at G0/G1 and G2/M accompanied induction of senescence‐like phenotypes (SLPs). Most importantly, the effect of NaB on senescence induction was not coupled with the predominance of hypophosphorylated pRb forms in the cervical cancer cells. This suggested that NaB had the potential to elicit SLPs through p21‐mediated withdrawal from cell cycle progression. The consequences of p21 induction were manifold. The effects of NaB on gynecologic cancer cell growth indicated its potential use in cancer treatment. NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence. © 2001 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ijc.1448 |
| format | Article |
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The arrest of cells at the G1 checkpoint accounted for this effect. NaB‐mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation. To demonstrate the role of pRb regulation by p21, we measured the sensitivity to NaB of cervical cancer cells in which pRb had been inactivated by HPV E7. The cervical cancer cells displayed a sensitivity in NaB‐mediated G2/M arrest in addition to their sensitivity in G0/G1 arrest. Arrest at G0/G1 and G2/M accompanied induction of senescence‐like phenotypes (SLPs). Most importantly, the effect of NaB on senescence induction was not coupled with the predominance of hypophosphorylated pRb forms in the cervical cancer cells. This suggested that NaB had the potential to elicit SLPs through p21‐mediated withdrawal from cell cycle progression. The consequences of p21 induction were manifold. The effects of NaB on gynecologic cancer cell growth indicated its potential use in cancer treatment. NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence. © 2001 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.1448</identifier><identifier>PMID: 11668507</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Butyrates - pharmacology ; Cell Cycle - drug effects ; Cellular Senescence - drug effects ; Chemotherapy ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins - biosynthesis ; Female ; Genital Neoplasms, Female - drug therapy ; Genital Neoplasms, Female - pathology ; Humans ; Medical sciences ; Mice ; Mice, Inbred BALB C ; p16 ; p21 ; p53 ; Pharmacology. Drug treatments ; Phenotype ; pRb ; senescence ; sodium butyrate ; Tumor Cells, Cultured</subject><ispartof>International journal of cancer, 2001-10, Vol.94 (2), p.257-267</ispartof><rights>Copyright © 2001 Wiley‐Liss, Inc.</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2001 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3818-9cc11db83061b75e5e53699cb05e214b6849535e13699c72efad76584e4c1ae53</citedby><cites>FETCH-LOGICAL-c3818-9cc11db83061b75e5e53699cb05e214b6849535e13699c72efad76584e4c1ae53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fijc.1448$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.1448$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14128786$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11668507$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Terao, Yasuhisa</creatorcontrib><creatorcontrib>Nishida, Jun‐ichi</creatorcontrib><creatorcontrib>Horiuchi, Shinji</creatorcontrib><creatorcontrib>Rong, Fengnian</creatorcontrib><creatorcontrib>Ueoka, Yousuke</creatorcontrib><creatorcontrib>Matsuda, Takao</creatorcontrib><creatorcontrib>Kato, Hidenori</creatorcontrib><creatorcontrib>Furugen, Yoshiaki</creatorcontrib><creatorcontrib>Yoshida, Koyo</creatorcontrib><creatorcontrib>Kato, Kiyoko</creatorcontrib><creatorcontrib>Wake, Norio</creatorcontrib><title>Sodium butyrate induces growth arrest and senescence‐like phenotypes in gynecologic cancer cells</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>We demonstrated here the growth‐suppressing effects of sodium butyrate (NaB) on human endometrial and ovarian cancer cells. The arrest of cells at the G1 checkpoint accounted for this effect. NaB‐mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation. To demonstrate the role of pRb regulation by p21, we measured the sensitivity to NaB of cervical cancer cells in which pRb had been inactivated by HPV E7. The cervical cancer cells displayed a sensitivity in NaB‐mediated G2/M arrest in addition to their sensitivity in G0/G1 arrest. Arrest at G0/G1 and G2/M accompanied induction of senescence‐like phenotypes (SLPs). Most importantly, the effect of NaB on senescence induction was not coupled with the predominance of hypophosphorylated pRb forms in the cervical cancer cells. This suggested that NaB had the potential to elicit SLPs through p21‐mediated withdrawal from cell cycle progression. The consequences of p21 induction were manifold. The effects of NaB on gynecologic cancer cell growth indicated its potential use in cancer treatment. NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence. © 2001 Wiley‐Liss, Inc.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Butyrates - pharmacology</subject><subject>Cell Cycle - drug effects</subject><subject>Cellular Senescence - drug effects</subject><subject>Chemotherapy</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclins - biosynthesis</subject><subject>Female</subject><subject>Genital Neoplasms, Female - drug therapy</subject><subject>Genital Neoplasms, Female - pathology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>p16</subject><subject>p21</subject><subject>p53</subject><subject>Pharmacology. Drug treatments</subject><subject>Phenotype</subject><subject>pRb</subject><subject>senescence</subject><subject>sodium butyrate</subject><subject>Tumor Cells, Cultured</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MtKAzEUBuAgiq1V8AkkG8XN1Jy5ZpZSvFQKLtT1kMmcaVPnZjJDmZ2P4DP6JKbtQFeSRSD5OJefkEtgU2DMvVNrOQXf50dkDCyOHOZCcEzG9os5EXjhiJwZs2YMIGD-KRkBhCEPWDQm6Vudqa6kadf2WrRIVZV1Eg1d6nrTrqjQGk1LRZVRgxUaiZXE3--fQn0ibVZY1W3fWK4quuwrlHVRL5WkUlimqcSiMOfkJBeFwYvhnpCPx4f32bOzeH2az-4XjvQ4cCeWEiBLucdCSKMA7fHCOJYpC9AFPw25HwdegLB7jVzMRRaFAffRlyAsnpCbfd1G11-dnTopldlOICqsO5NEruvadGILb_dQ6toYjXnSaFUK3SfAkm2eic0z2eZp6dVQs0tLzA5wCNCC6wEII0WRa7u4Mgfng8sjHlrn7N1GFdj_2zCZv8x2jf8A_nKNNQ</recordid><startdate>20011015</startdate><enddate>20011015</enddate><creator>Terao, Yasuhisa</creator><creator>Nishida, Jun‐ichi</creator><creator>Horiuchi, Shinji</creator><creator>Rong, Fengnian</creator><creator>Ueoka, Yousuke</creator><creator>Matsuda, Takao</creator><creator>Kato, Hidenori</creator><creator>Furugen, Yoshiaki</creator><creator>Yoshida, Koyo</creator><creator>Kato, Kiyoko</creator><creator>Wake, Norio</creator><general>John Wiley & Sons, Inc</general><general>Wiley-Liss</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20011015</creationdate><title>Sodium butyrate induces growth arrest and senescence‐like phenotypes in gynecologic cancer cells</title><author>Terao, Yasuhisa ; Nishida, Jun‐ichi ; Horiuchi, Shinji ; Rong, Fengnian ; Ueoka, Yousuke ; Matsuda, Takao ; Kato, Hidenori ; Furugen, Yoshiaki ; Yoshida, Koyo ; Kato, Kiyoko ; Wake, Norio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3818-9cc11db83061b75e5e53699cb05e214b6849535e13699c72efad76584e4c1ae53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Butyrates - pharmacology</topic><topic>Cell Cycle - drug effects</topic><topic>Cellular Senescence - drug effects</topic><topic>Chemotherapy</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclins - biosynthesis</topic><topic>Female</topic><topic>Genital Neoplasms, Female - drug therapy</topic><topic>Genital Neoplasms, Female - pathology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>p16</topic><topic>p21</topic><topic>p53</topic><topic>Pharmacology. Drug treatments</topic><topic>Phenotype</topic><topic>pRb</topic><topic>senescence</topic><topic>sodium butyrate</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Terao, Yasuhisa</creatorcontrib><creatorcontrib>Nishida, Jun‐ichi</creatorcontrib><creatorcontrib>Horiuchi, Shinji</creatorcontrib><creatorcontrib>Rong, Fengnian</creatorcontrib><creatorcontrib>Ueoka, Yousuke</creatorcontrib><creatorcontrib>Matsuda, Takao</creatorcontrib><creatorcontrib>Kato, Hidenori</creatorcontrib><creatorcontrib>Furugen, Yoshiaki</creatorcontrib><creatorcontrib>Yoshida, Koyo</creatorcontrib><creatorcontrib>Kato, Kiyoko</creatorcontrib><creatorcontrib>Wake, Norio</creatorcontrib><collection>Pascal-Francis</collection><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>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Terao, Yasuhisa</au><au>Nishida, Jun‐ichi</au><au>Horiuchi, Shinji</au><au>Rong, Fengnian</au><au>Ueoka, Yousuke</au><au>Matsuda, Takao</au><au>Kato, Hidenori</au><au>Furugen, Yoshiaki</au><au>Yoshida, Koyo</au><au>Kato, Kiyoko</au><au>Wake, Norio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sodium butyrate induces growth arrest and senescence‐like phenotypes in gynecologic cancer cells</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2001-10-15</date><risdate>2001</risdate><volume>94</volume><issue>2</issue><spage>257</spage><epage>267</epage><pages>257-267</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>We demonstrated here the growth‐suppressing effects of sodium butyrate (NaB) on human endometrial and ovarian cancer cells. The arrest of cells at the G1 checkpoint accounted for this effect. NaB‐mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation. To demonstrate the role of pRb regulation by p21, we measured the sensitivity to NaB of cervical cancer cells in which pRb had been inactivated by HPV E7. The cervical cancer cells displayed a sensitivity in NaB‐mediated G2/M arrest in addition to their sensitivity in G0/G1 arrest. Arrest at G0/G1 and G2/M accompanied induction of senescence‐like phenotypes (SLPs). Most importantly, the effect of NaB on senescence induction was not coupled with the predominance of hypophosphorylated pRb forms in the cervical cancer cells. This suggested that NaB had the potential to elicit SLPs through p21‐mediated withdrawal from cell cycle progression. The consequences of p21 induction were manifold. The effects of NaB on gynecologic cancer cell growth indicated its potential use in cancer treatment. NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence. © 2001 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>11668507</pmid><doi>10.1002/ijc.1448</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of cancer, 2001-10, Vol.94 (2), p.257-267 |
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| subjects | Animals Antineoplastic agents Biological and medical sciences Butyrates - pharmacology Cell Cycle - drug effects Cellular Senescence - drug effects Chemotherapy Cyclin-Dependent Kinase Inhibitor p21 Cyclins - biosynthesis Female Genital Neoplasms, Female - drug therapy Genital Neoplasms, Female - pathology Humans Medical sciences Mice Mice, Inbred BALB C p16 p21 p53 Pharmacology. Drug treatments Phenotype pRb senescence sodium butyrate Tumor Cells, Cultured |
| title | Sodium butyrate induces growth arrest and senescence‐like phenotypes in gynecologic cancer cells |
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