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*** of *** enhances prost.t. cancer chemoresist.nce via Not.h signaling

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Chinese Journal of Cancer 2017年第3期36卷 150-162页

作者： Wenchu Wang Lihui Wang At.ushi Mizokami Junlin Shi Chunlin Zou Jinlu Dai evan t. keller Yi Lu Jian Zhang Cent.r for t.anslat.onal Medicine Guangxi Medical University 12th FloorMedical Science Research Building No. 22 Shuangyong Road NanningGuangxi 530021 P. R. China Key Laborat.ry of Longevit. and Ageingrelat.d Diseases Ministry of Education Nanning Guangxi 530021 P. R. China Depart.ent.of Urology and Pat.ology School of Medicine University of Michigan Ann Arbor MI 48109 USA Depart.ent.of Urology Graduate School of Medical Sciences Kanazawa University Kanazawa 920.1192 Japan Depart.ent.of Biology and School of Medicine Southern University of Science and Technology Shenzhen Guangdong 518055 P. R. China Depart.ent.of Urology University of Pittsburgh School of Medicine Pittsburgh PA 15232 USA

Background:t.e chemoresist.nce of prost.t. cancer(PCa)is invariably associat.d wit. t.e aggressiveness and met.st.sis of t.is *** emerging evidence indicat.s t.at.t.e epit.elial-t.-mesenchymal t.ansit.on(EMt.may play pivot.l roles in t.e development.of chemoresist.nce and *** a hallmark of EMt.E-cadherin is suggest.d t. be a key marker in t.e development.of ***,t.e molecular mechanisms underlying PCa chemoresist.nce remain *** current.st.dy aimed t. explore t.e associat.on bet.een EMt.and chemoresist.nce in PCa as well as whet.er changing t.e expression of E-cadherin would affect.PCa ***:Parent.l PC3 and DU145 cells and t.eir chemoresist.nt.PC3-t. R and DU145-t. R cells were ***3-t. R and DU145-t. R cells were t.ansfect.d wit. E-cadherin-expressing lent.virus t. overexpress E-cadherin;PC3 and DU145 cells were t.ansfect.d wit. small int.rfering RNA t. silence *** of EMt.phenot.pe-relat.d markers and signaling pat.ways were assessed by West.rn blot.ing and quant.t.t.ve real-t.me polymerase chain *** cell migrat.on,invasion,and colony format.on were t.en evaluat.d by wound healing,t.answell,and colony format.on assays,*** drug sensit.vit. was evaluat.d using Mt. ***:Chemoresist.nt.PC3-t. R and DU145-t. R cells exhibit.d an invasive and met.st.t.c phenot.pe t.at.associat.d wit. EMt.including t.e down-regulat.on of E-cadherin and up-regulat.on of Viment.n,Snail,and N-cadherin,comparing wit. t.at.of parent.l PC3 and DU145 *** E-cadherin was overexpressed in PC3-t. R and DU145-t. R cells,t.e expression of Viment.n and Claudin-1 was down-regulat.d,and t.mor cell migrat.on and invasion were *** part.cular,t.e sensit.vit. t. paclit.xel was react.vat.d in E-cadherin-overexpressing PC3-t. R and DU145-t. R *** E-cadherin expression was silenced in parent.l PC3 and DU145 cells,t.e expression of Viment.n and Snail was up-regulat.d,and,pa

关键词： Epit.elial-t.-mesenchymal t.ansit.on E-cadherin Chemoresist.nce Not.h signaling Prost.t. cancer

Raf Kinase Inhibit.r Prot.in (RKIP) and It. Role in Cancer

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中国肺癌杂志 2009年第6期12卷 I0006-I0006页

作者： evan t. keller Universit. of Michigan Ann Arbor MI USA

Raf kinase inhibit.r prot.in (RKIP) was originally ident.fied as a prot.in t.at.bound membrane phospholipids and was named

关键词： RKIP 肺癌临床摄制剂癌细胞

t.rget.ng CC Chemokine Ligand 2 (CCL2) for Cancer Skelet.l Met.st.sis

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中国肺癌杂志 2009年第6期 7-7页

作者： Eva COREY At.ushi MIZOKAMI evan t. keller Kennet. J. PIENt. Depart.ent.of Urology Universit. of Washingt.n Depart.ent.of Urology Kanazawa Universit. Graduat. School of Medical Sciences Depart.ent.of Int.rnal Medicine and Urology Universit. of Michigan

Prost.t., breast. and lung cancer preferent.ally met.st.size t. bone result.ng in bone lesions and t.us high mort.lit.. However, t.e mechanisms

关键词： for Cancer Skelet.l Met.st.sis bone CCL2 t.rget.ng CC Chemokine Ligand 2

Prost.t. cancer cells met.st.size t. t.e hemat.poiet.c st.m cell niche in bone

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Asian Journal of Andrology 2011年第4期13卷 622-623页

作者： evan t.keller Depart.ent. of UroJogy and Pat.ology University of Michigan Ann Arbor MI 48109 USA

t.e majorit. of men wit. advanced prost.t. cancer develop bone met.st.ses as opposed t. met.st.ses at.ot.er sit.s. It.has been unclear why prost.t. cancer select.vely met.st.sizes t. and proliferat.s in bone. Recent.y, Shiozawa et.al. delineat.d a mechanism t.at.may account.for t.e est.blishment.of prost.t. cancer in bone. Specifically, t.ey ident.fied t.at.prost.t. cancer cells compet. wit. hemat.poiet.c st.m cells （HSC） for t.e ost.oblast.in t.e HSC niche of t.e bone. Defining t.e mechanisms t.rough which prost.t. cancer cells est.blish t.emselves in bone is crit.cal t.wards developing effect.ve t.erapeut.c st.at.gies t. prevent.or t.rget.bone met.st.ses.

关键词： Prost.t. hemat.poiet.c

SPDEF： a molecular swit.h for E-cadherin expression t.at.promot.s prost.t. cancer met.st.sis

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Asian Journal of Andrology 2013年第5期15卷 584-585页

作者： Mary Osisami evan t.keller Depart.ent.of Urology University of Michigan AnnArbor M148105 USA

In order t. design effect.ve t.erapies for prost.t. cancer, a clear underst.nding of mechanisms t.at.cont.ibut. t. various component. of prost.t. cancer progression is necessary. St.dy of met.st.sis suppressor genes, i.e., genes t.at.can inhibit.met.st.sis, is an import.nt.field of st.dy t.at.can lead t. ident.ficat.on of t.erapeut.c t.rget. t. diminish met.st.sis.

关键词： SPDEF a molecular swit.h met.st.sis

t.rget.ng CC Chemokine Ligand 2 (CCL2) for Cancer Skelet.l Met.st.sis

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中国肺癌杂志 2009年第6期12卷 I0007-I0007页

作者： Yi LU Cai ZHONG Qiuyan CHEN Eva COREY Zhi YAO At.ushi MIZOKAMI Qinghua ZHOU evan t. keller Kennet. J. PIENt. Jian ZHANG Depart.ent.of Medicine University of Pittsburgh Pittsburgh PA 15240 Depart.ent.of Immunology Tianjin Medical University Tianjinj China Laborat.ry of Clinical Chemist.y Tianjin Chest Hospital Tianjin China Depart.ent.of Nasopharyngeal Carcinoma Cancer Center Sun Yatsen University Guangzhou China Depart.ent.of Urology University of Washington Seattle WA 98195 Depart.ent.of Urology Kanazawa University Graduate School of Medical Sciences Kanazawa Japan t.anjin Lung Cancer Inst.t.t. Tianjin Medical University General Hospital Tianjin China Depart.ent.of Int.rnal Medicine and Urology University of Michigan Ann Arbor MI48105

Prost.t., breast. and lung cancer preferent.ally met.st.size t. bone result.ng in bone lesions and t.us high mort.lit.. However, t.e

关键词：癌细胞 CCL2 肿瘤治疗化疗

Wnt.a:funct.ons and implicat.ons in cancer

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Chinese Journal of Cancer 2015年第12期34卷 554-562页

作者： Sha He Yi Lu Xia Liu Xin Huang evan t.keller Chao-Nan Qian Jian Zhang Key Laborat.ry of Longevit. and Ageing-relat.d Diseases Ministry of Education Cent.r for t.anslat.onal Medicine Guangxi Medical University Depart.ent.of Urology and Pat.ology School of MedicineUniversity of Michigan Depart.ent.of Nasopharyngeal Carcinoma Sun Yat-sen University Cancer CenterState Key Laboratory of Oncology in South ChinaCollaborative Innovation Center of Cancer Medicine

Wnt.a,one of Wnt.family members,plays key roles in regulat.ng pleiot.opic cellular funct.ons,including self-renewal,proliferat.on,different.at.on,and *** evidence has suggest.d t.at.Wnt. a promot.s or suppresses t.mor progression via t.e canonical Wnt.signaling pat.way depending on cancer *** addit.on,t.e roles of Wnt. a signaling can be inhibit.d by mult.ple prot.ins or ***,we summarize t.e lat.st.findings on Wnt. a as an import.nt.t.erapeut.c t.rget.in cancer.

关键词： Wnt.a,t.e Wnt signaling pat.way, Cancer

Met.ormin t.rget. mult.ple signaling pat.ways in cancer

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Chinese Journal of Cancer 2017年第7期36卷 289-297页

作者： Yong Lei Yanhua Yi Yang Liu Xia Liu evan t.keller Chao.Nan Qian Jian Zhang Yi Lu Key Laborat.ry of Longevit. and Ageing.relat.d Diseases Ministry of EducationNanning 530021GuangxiP.R.China Cent.r for t.anslat.onal Medicine Guangxi Medical University14th FloorPharmacology and Biomedical Sciences BuildingNo.22 Shuangyong RoadNanning 530021GuangxiP.R.China School for Int.rnat.onal Educat.on Guangxi Medical UniversityNanning 530021GuangxiP.R.China Depart.ent.of Urology and Pat.ology School of MedicineUniversity of MichiganAnn ArborMI 48109USA Depart.ent.of Nasopharyngeal Carcinoma State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060GuangdongP.R.China

Met.ormin,an inexpensive and well-t.lerat.d oral agent.commonly used in t.e first.line t.eat.ent.of t.pe 2 diabet.s,has become t.e focus of int.nse research as a candidat. ant.cancer ***,we discuss t.e pot.nt.al of met.ormin in cancer t.erapeut.cs,part.cularly it. funct.ons in mult.ple signaling pat.ways,including AMP-act.vat.d prot.in kinase,mammalian t.rget.of rapamycin,insulin-like growt. fact.r,c-Jun N-t.rminal kinase/mit.gen-act.vat.d prot.in kinase(p38 MARK),human epidermal growt. fact.r recept.r-2,and nuclear fact.r kappaB *** addit.on,cut.ing-edge t.rget.ng of cancer st.m cells by met.ormin is summarized.

关键词： Met.ormin Signaling pat.way Cancer st.m cell Cancer

Prost.t. cancer t.nds t. met.st.size in t.e bone-mimicking microenvironment.via act.vat.ng NF-κB signaling

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t.e Journal of Biomedical Research 2018年第5期32卷 343-353页

作者： Haibo t.ng Chunlin Zou Siyuan Qin Jie Meng evan t.keller Jian Zhang Yi Lu Key Laborat.ry of Longevit. and Aging-relat.d Diseases Guangxi Medical University Ministry of Education Nanning Guangxi 530021 China Sout.ern Universit. of Science and t.chnology School of Medicine Shenzhen Guangdong 518055 China Depart.ent.of Pat.ology and Int.rnal Medicine University of Michigan Ann Arbor MI 48109 USA

Prost.t. cancer preferent.ally met.st.sizes t. t.e bone. However, t.e underlying molecular mechanisms are st.ll unclear. t. explore t.e effect. of a bone-mimicking microenvironment.on PC3 prost.t. cancer cell growt. and met.st.sis, we used ost.oblast.different.at.on medium（ODM; minimal essent.al medium alpha supplement.d wit. L-ascorbic acid） t. mimic t.e bone microenvironment. PC3 cells grown in ODM underwent.epit.elial-mesenchymal t.ansit.on and showed enhanced colony format.on, migrat.on, and invasion abilit.es compared t. t.e cells grown in normal medium. PC3 cells grown in ODM showed enhanced met.st.sis when inject.d in mice. A screening of signaling pat.ways relat.d t. invasion and met.st.sis revealed t.at.t.e NF-κB pat.way was act.vat.d, which could be reversed by Bay 11-7082, a NF-κB pat.way inhibit.r. t.ese result. indicat. t.at.t.e cells in different.cult.re condit.ons manifest.d significant.y different.biological behaviors and t.e NF-κB pat.way is a pot.nt.al t.erapeut.c t.rget.for prost.t. cancer bone met.st.sis.

关键词： prost.t. cancer met.st.sis NF-κB Bay 11-7082 EMt