Epithelial-to-Mesenchymal Transition in Pancreatic Adenocarcinoma

被引：61

作者：

Cano, Carla ^{[1
]}

Motoo, Yoshiharu ^{[2
]}

Iovanna, Juan L. ^{[1
]}

机构：

[1] INSERM, Cell Stress U624, Biol Pancreas Stress Lab, F-13258 Marseille, France

[2] Kanazawa Med Univ, Dept Med Oncol, Kanazawa, Ishikawa, Japan

来源：

THESCIENTIFICWORLDJOURNAL | 2010年 / 10卷

关键词：

cancer; pancreas; epithelial-to-mesenchymal transition; TGFbeta; metastasis; HEPATOCYTE GROWTH-FACTOR; CANCER CELLS; MIR-200; FAMILY; UP-REGULATION; EXPRESSION; SNAIL; INDUCTION; INVASIVENESS; PROGRESSION; PHENOTYPE;

D O I：

10.1100/tsw.2010.183

中图分类号：

X [环境科学、安全科学];

学科分类号：

083001 [环境科学];

摘要：

Epithelial to mesenchymal transition (EMT) is a physiologic process that allows morphological and genetic changes of carcinoma cells from an epithelial to a mesenchymal phenotype, which is the basis of the high metastatic potential of pancreatic cancer cells. EMT is triggered by various tumor microenvironmental factors, including cytokines, growth factors, and chemotherapeutic agents. This review summarizes the state-of-the-art knowledge on the molecular mechanisms that support pancreatic cancer EMT and the evidences that support its involvement in invasiveness/aggressiveness, and the drug resistance of pancreatic cancer cells.

引用

页码：1947 / 1957

页数：11

共 46 条

[1]

Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma [J].

Aguirre, AJ ;

Bardeesy, N ;

Sinha, M ;

Lopez, L ;

Tuveson, DA ;

Horner, J ;

Redston, MS ;

DePinho, RA .

GENES & DEVELOPMENT, 2003, 17 (24) :3112-3126

[2]

Epithelial to Mesenchymal Transition Contributes to Drug Resistance in Pancreatic Cancer [J].

Arumugam, Thiruvengadam ;

Ramachandran, Vijaya ;

Fournier, Keith F. ;

Wang, Huamin ;

Marquis, Lauren ;

Abbruzzese, James L. ;

Gallick, Gary E. ;

Logsdon, Craig D. ;

McConkey, David J. ;

Choi, Woonyoung .

CANCER RESEARCH, 2009, 69 (14) :5820-5828

[3]

Both p16Ink4a and the p19Arf-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse [J].

Bardeesy, N ;

Aguirre, AJ ;

Chu, GC ;

Cheng, KH ;

Lopez, LV ;

Hezel, AF ;

Feng, B ;

Brennan, C ;

Weissleder, R ;

Mahmood, U ;

Hanahan, D ;

Redston, MS ;

Chin, L ;

DePinho, RA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (15) :5947-5952

[4]

Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer [J].

Bardeesy, Nabeel ;

Cheng, Kuang-hung ;

Berger, Justin H. ;

Chu, Gerald C. ;

Pahler, Jessica ;

Olson, Peter ;

Hezel, Aram F. ;

Horner, James ;

Lauwers, Gregory Y. ;

Hanahan, Douglas ;

DePinho, Ronald A. .

GENES & DEVELOPMENT, 2006, 20 (22) :3130-3146

[5]

A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells [J].

Burk, Ulrike ;

Schubert, Joerg ;

Wellner, Ulrich ;

Schmalhofer, Otto ;

Vincan, Elizabeth ;

Spaderna, Simone ;

Brabletz, Thomas .

EMBO REPORTS, 2008, 9 (06) :582-589

[6]

Tyrosine kinase receptor RON in human pancreatic cancer - Expression, function, and validation as a target [J].

Camp, E. Ramsay ;

Yang, Anthony ;

Gray, Mike J. ;

Fan, Fan ;

Hamilton, Stanley R. ;

Evans, Douglas B. ;

Hooper, Andrea T. ;

Pereira, Daniel S. ;

Hicklin, Daniel J. ;

Ellis, Lee M. .

CANCER, 2007, 109 (06) :1030-1039

[7]

Redox mechanisms switch on hypoxia-dependent epithelial-mesenchymal transition in cancer cells [J].

Cannito, Stefania ;

Novo, Erica ;

Compagnone, Alessandra ;

Valfre di Bonzo, Lorenzo ;

Busletta, Chiara ;

Zamara, Elena ;

Paternostro, Claudia ;

Povero, Davide ;

Bandino, Andrea ;

Bozzo, Francesca ;

Cravanzola, Carlo ;

Bravoco, Vittoria ;

Colombatto, Sebastiano ;

Parola, Maurizio .

CARCINOGENESIS, 2008, 29 (12) :2267-2278

[8]

Hepatocyte Growth Factor Activator Inhibitor Type 1 Regulates Epithelial to Mesenchymal Transition through Membrane-Bound Serine Proteinases [J].

Cheng, Haixia ;

Fukushima, Tsuyoshi ;

Takahashi, Nobuyasu ;

Tanaka, Hiroyuki ;

Kataoka, Hiroaki .

CANCER RESEARCH, 2009, 69 (05) :1828-1835

[9]

EBERT M, 1994, CANCER RES, V54, P5775

[10]

Ellenrieder V, 2001, CANCER RES, V61, P4222

← 1 2 3 4 5 →