Forced Expression of miR-143 Represses ERK5c-Myc and p68p72 Signaling in Concert with miR-145 in Gut Tumors of ApcMin Mice 英文参考文献.docVIP

下载本文档

6
0
约4.8万字
约 12页
2017-05-11 发布于上海
举报
版权申诉

Forced Expression of miR-143 Represses ERK5c-Myc and p68p72 Signaling in Concert with miR-145 in Gut Tumors of ApcMin Mice 英文参考文献.doc

1、本文档共12页，可阅读全部内容。
2、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。
3、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
4、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
5、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
6、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
7、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
8、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

Forced Expression of miR-143 Represses ERK5c-Myc and p68p72 Signaling in Concert with miR-145 in Gut Tumors of ApcMin Mice 英文参考文献

ForcedExpressionofmiR-143RepressesERK5/c-Mycand p68/p72SignalinginConcertwithmiR-145inGut TumorsofApcMin Mice YujiTakaoka1.,YukoShimizu1.,HitokiHasegawa2,3,YasuoOuchi2,ShanlouQiao1,MikiNagahara2, MasatoshiIchihara1,Jiing-DwanLee4,KoichiAdachi5,MichinariHamaguchi3,TakashiIwamoto1,2* 1Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Aichi, Japan, 2The Center for Education in Laboratory Animal Research,ChubuUniversity,Kasugai,Aichi,Japan,3DivisionofCancerBiology,NagoyaUniversityGraduateSchoolofMedicine,Nagoya,Aichi,Japan,4Departmentof ImmunologyandMicrobialScience,TheScrippsResearchInstitute,LaJolla,California,UnitedStatesofAmerica,5RadioisotopeResearchCenterMedicalDivision,Nagoya UniversityGraduateSchoolofMedicine,Nagoya,Aichi,Japan Abstract Recently,miR-143andmiR-145havebeenshowntobelongtoasubsetofmicroRNAswhoseexpressioniscontrolledbya complex of a tumor suppressor p53 and DEAD-box RNA helicase subunits p68/p72. While accumulating studies have acknowledgedthatbothmiRNAsfunctionastumorsuppressorsandaresimilarlyregulated,evidenceoftheircoordinated actionagainsttumorigenesishasbeenpoorlypresented.Herein,weestablishtransgenicmicethatexpressmiR-143under mice, the development of tumors in the small Min/+ the control of the CAG regulatory unit. When crossbred with Apc intestinesissignificantlyattenuated.Inthetransgenicsmallintestinetumors,theendogenousmiR-145isalsoenhanced andtheexpressionofc-Mycandp68/p72,bothofwhichhavebeenreportedtobepivotalforguttumordevelopment,is suppressed,correspondingtothedownregulationofERK5.WedemonstratethatthecombinationofmiR-143andmiR-145 inhibitstheexpressionofc-Mycinhumancoloncancercells,whereasmiR-145retardsthatofp72.Moreover,weshowthe possibilitiesthatmiR-145modulatesp72expressionthroughits39untranslatedregionandthatc-Mycdownregulationis involved in both p68 suppression and miR-145 induction. These findings suggest that forced expression of miR-143, probablyinteractingwithendogenousmiR-