Transición epitelial-mesenquimal en la progresión del adenocarcinoma prostático

Autores/as

  • Inés Benedetti Universidad de Cartagena
  • Niradiz Reyes Universidad de Cartagena

DOI:

https://doi.org/10.17533/udea.iatreia.v28n4a07

Palabras clave:

transición epitelial-mesenquimal, adhesión celular, metástasis , adenocarcinoma prostático

Resumen

Mundialmente, el adenocarcinoma prostático es el segundo cáncer diagnosticado en hombres y las metástasis son su principal complicación; se ha descrito la participación en su desarrollo de la transición epitelial-mesenquimal (TEM) proceso fundamental durante el desarrollo embrionario, la remodelación tisular y la cicatrización, que implica pérdida de las propiedades adhesivas y la polaridad epitelial y adquisición del fenotipo mesenquimal que aumenta la movilidad celular individual y permite el desarrollo de características invasivas. Este cambio en el comportamiento celular es mediado por una regulación molecular compleja en la que participa un gran número de vías de señalización, algunas actuando en forma independiente y otras interconectadas; la mayoría converge en el control de la expresión de la E-cadherina, cuya subregulación es el evento molecular clave en este proceso. Diversos estudios señalan una relación estrecha entre la TEM y el desarrollo y progresión de metástasis en carcinomas, pero ha sido menos ampliamente estudiada en el adenocarcinoma prostático. Los objetivos de esta revisión fueron: describir las bases moleculares y morfológicas de este proceso biológico y analizar la influencia de sus reguladores en la adquisición del fenotipo agresivo por las células tumorales, específicamente en lo que tiene que ver con la progresión del adenocarcinoma prostático. 

|Resumen
= 1103 veces | PDF
= 799 veces|

Descargas

Los datos de descargas todavía no están disponibles.

Biografía del autor/a

Inés Benedetti, Universidad de Cartagena

MD. Patóloga. Grupo de Histopatología, Facultad de Medicina, Universidad de Cartagena, Colombia.

Niradiz Reyes, Universidad de Cartagena

PhD. Grupo de Genética y Biología Molecular, Facultad de Medicina, Universidad de Cartagena, Colombia.

Citas

Siegel R, Ma J, Zou Z, Jemal A. Cancer statistics, 2014. CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29.

Armstrong AJ, Freedland SJ, Garcia-Blanco M. Epithelial-mesenchymal transition in prostate cancer: providing new targets for therapy. Asian J Androl. 2011 Mar;13(2):179-80.

Yao D, Dai C, Peng S. Mechanism of the mesenchymal-epithelial transition and its relationship with metastatic tumor formation. Mol Cancer Res. 2011 Dec;9(12):1608-20.

Steeg PS. Tumor metastasis: mechanistic insights and clinical challenges. Nat Med. 2006 Aug;12(8):895-904.

Guarino M, Rubino B, Ballabio G. The role of epithelial-mesenchymal transition in cancer pathology. Pathology. 2007 Jun;39(3):305-18.

Trimboli AJ, Fukino K, de Bruin A, Wei G, Shen L, Tanner SM, et al. Direct evidence for epithelial-mesenchymal transitions in breast cancer. Cancer Res. 2008 Feb;68(3):937-45.

Deep G, Jain AK, Ramteke A, Ting H, Vijendra KC, Gangar SC, et al. SNAI1 is critical for the aggressiveness of prostate cancer cells with low E-cadherin. Mol Cancer. 2014 Feb;13:37.

Frisch SM, Schaller M, Cieply B. Mechanisms that link the oncogenic epithelial-mesenchymal transition to suppression of anoikis. J Cell Sci. 2013 Jan;126(Pt 1):21-9.

Micalizzi DS, Farabaugh SM, Ford HL. Epithelial-mesenchymal transition in cancer: parallels between normal development and tumor progression. J Mammary Gland Biol Neoplasia. 2010 Jun;15(2):117-34.

Hay ED. The mesenchymal cell, its role in the embryo, and the remarkable signaling mechanisms that create it. Dev Dyn. 2005 Jul;233(3):706-20.

(11.) Huang RY, Guilford P, Thiery JP. Early events in cell adhesion and polarity during epithelial-mesenchymal transition. J Cell Sci. 2012 Oct;125(Pt 19):4417-22.

(12.) Feigin ME, Muthuswamy SK. Polarity proteins regulate mammalian cell-cell junctions and cancer pathogenesis. Curr Opin Cell Biol. 2009 Oct;21(5):694-700.

(13.) Gumbiner BM. Cell adhesion: the molecular basis of tissue architecture and morphogenesis. Cell. 1996 Feb;84(3):345-57.

(14.) Kemler R. From cadherins to catenins: cytoplasmic protein interactions and regulation of cell adhesion. Trends Genet. 1993 Sep;9(9):317-21.

(15.) Peinado H, Portillo F, Cano A. Transcriptional regula-tion of cadherins during development and carcino-genesis. Int J Dev Biol. 2004;48(5-6):365-75.

(16.) Lamouille S, Xu J, Derynck R. Molecular mechanisms of epithelial-mesenchymal transition. Nat Rev Mol Cell Biol. 2014 Mar;15(3):178-96.

(17.) Jaggi M, Johansson SL, Baker JJ, Smith LM, Galich A, Balaji KC. Aberrant expression of E-cadherin and beta-catenin in human prostate cancer. Urol Oncol. 2005 Nov-Dec;23(6):402-6.

(18.) Fidler IJ. Critical determinants of metastasis. Semin Cancer Biol. 2002 Apr;12(2):89-96.

(19.) Tomita K, van Bokhoven A, van Leenders GJ, Ruijter ET, Jansen CF, Bussemakers MJ, et al. Cadherin switching in human prostate cancer progression. Cancer Res. 2000 Jul;60(13):3650-4.

(20.) Tiwari N, Gheldof A, Tatari M, Christofori G. EMT as the ultimate survival mechanism of cancer cells. Semin Cancer Biol. 2012 Jun;22(3):194-207.

(21.) Kalluri R, Weinberg RA. The basics of epithelial-mesenchymal transition. J Clin Invest. 2009 Jun;119(6):1420-8.

(22.) Hay ED. An overview of epithelio-mesenchymal transformation. Acta Anat (Basel). 1995;154(1):8-20.

(23.) Acloque H, Thiery JP, Nieto MA. The physiology and pathology of the EMT. Meeting on the epithelial-mesenchymal transition. EMBO Rep. 2008 Apr;9(4):322-6.

(24.) Shook D, Keller R. Mechanisms, mechanics and function of epithelial-mesenchymal transitions in early development. Mech Dev. 2003 Nov;120(11):1351-83.

(25.) Yilmaz M, Christofori G. EMT, the cytoskeleton, and cancer cell invasion. Cancer Metastasis Rev. 2009 Jun;28(1-2):15-33.

(26.) Lee JM, Dedhar S, Kalluri R, Thompson EW. The epithelial-mesenchymal transition: new insights in signaling, development, and disease. J Cell Biol. 2006 Mar;172(7):973-81.

(27.) Zhu QC, Gao RY, Wu W, Qin HL. Epithelial-mesenchymal transition and its role in the pathogenesis of colorectal cancer. Asian Pac J Cancer Prev. 2013;14(5):2689-98.

(28.) Leopold PL, Vincent J, Wang H. A comparison of epithelial-to-mesenchymal transition and re-epithelialization. Semin Cancer Biol. 2012 Oct;22(5-6):471-83.

(29.) Smith BN, Odero-Marah VA. The role of Snail in prostate cancer. Cell Adh Migr. 2012 Sep-Oct;6(5):433-41.

(30.) Murali AK, Norris JS. Differential expression of epithelial and mesenchymal proteins in a panel of prostate cancer cell lines. J Urol. 2012 Aug;188(2):632-8.

(31.) De Marzo AM, Knudsen B, Chan-Tack K, Epstein JI. Ecadherin expression as a marker of tumor aggressiveness in routinely processed radical prostatectomy specimens. Urology. 1999 Apr;53(4):707-13.

(32.) Whiteland H, Spencer-Harty S, Thomas DH, Davies C, Morgan C, Kynaston H, et al. Putative prognostic epithelial-to-mesenchymal transition biomarkers for aggressive prostate cancer. Exp Mol Pathol. 2013 Oct;95(2):220-6.

(33.) Sandig M, Voura EB, Kalnins VI, Siu CH. Role of cadherins in the transendothelial migration of me-lanoma cells in culture. Cell Motil Cytoskeleton. 1997;38(4):351-64.

(34.) Tran NL, Nagle RB, Cress AE, Heimark RL. N-Cadherin expression in human prostate carcinoma cell lines. An epithelial-mesenchymal transformation mediating adhesion withStromal cells. Am J Pathol. 1999 Sep;155(3):787-98.

(35.) Gravdal K, Halvorsen OJ, Haukaas SA, Akslen LA. A switch from E-cadherin to N-cadherin expression indicates epithelial to mesenchymal transition and is of strong and independent importance for the progress of prostate cancer. Clin Cancer Res. 2007 Dec;13(23):7003-11.

(36.) Jennbacken K, Tesan T, Wang W, Gustavsson H, Damber JE, Welén K. N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer. Endocr Relat Cancer. 2010 May;17(2):469-79.

(37.) Wang Y, Shang Y. Epigenetic control of epithelial-to-mesenchymal transition and cancer metastasis. Exp Cell Res. 2013 Jan;319(2):160-9.

(38.) Rubin MA, Mucci NR, Figurski J, Fecko A, Pienta KJ, Day ML. E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology. Hum Pathol. 2001 Jul;32(7):690-7.

(39.) Jennbacken K, Gustavsson H, Welén K, Vallbo C, Damber JE. Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity. Prostate. 2006 Nov;66(15):1631-40.

(40.) Bussemakers MJ, Van Bokhoven A, Tomita K, Jansen CF, Schalken JA. Complex cadherin expression in human prostate cancer cells. Int J Cancer. 2000 Feb;85(3):446-50.

(41.) Kallakury BV, Sheehan CE, Winn-Deen E, Oliver J, Fisher HA, Kaufman RP Jr, et al. Decreased expression of catenins (alpha and beta), p120 CTN, and E-cadherin cell adhesion proteins and E-cadherin gene promoter methylation in prostatic adenocarcinomas. Cancer. 2001 Dec;92(11):2786-95.

(42.) Vallorosi CJ, Day KC, Zhao X, Rashid MG, Rubin MA, Johnson KR, et al. Truncation of the beta-catenin bin-ding domain of E-cadherin precedes epithelial apop-tosis during prostate and mammary involution. J Biol Chem. 2000 Feb;275(5):3328-34.

(43.) Cano A, Pérez-Moreno MA, Rodrigo I, Locascio A, Blanco MJ, del Barrio MG, et al. The transcription fac-tor snail controls epithelial-mesenchymal transitions by repressing E-cadherin expression. Nat Cell Biol. 2000 Feb;2(2):76-83.

(44.) Medici D, Hay ED, Olsen BR. Snail and Slug promote epithelial-mesenchymal transition through betacatenin-T-cell factor-4-dependent expression of transforming growth factorbeta3. Mol Biol Cell. 2008 Nov;19(11):4875-87.

(45.) Comijn J, Berx G, Vermassen P, Verschueren K, van Grunsven L, Bruyneel E, et al. The two-handed E box binding zinc finger protein SIP1 downregula-tes E-cadherin and induces invasion. Mol Cell. 2001 Jun;7(6):1267-78.

(46.) Le Bras GF, Taubenslag KJ, Andl CD. The regulation of cell-cell adhesion during epithelial-mesenchymal transition, motility and tumor progression. Cell Adh Migr. 2012 Jul-Aug;6(4):365-73.

(47.) Stadler SC, Allis CD. Linking epithelial-to-mesenchy-mal-transition and epigenetic modifications. Semin Cancer Biol. 2012 Oct;22(5-6):404-10.

(48.) Mak P, Leav I, Pursell B, Bae D, Yang X, Taglienti CA, et al. ERbeta impedes prostate cancer EMT by destabilizing HIF-1alpha and inhibiting VEGF-mediated snail nuclear localization: implications for Gleason grading. Cancer Cell. 2010 Apr;17(4):319-32. Erratum in: Cancer Cell. 2010 Jun;17(6):622.

(49.) Odero-Marah VA, Wang R, Chu G, Zayzafoon M, Xu J, Shi C, et al. Receptor activator of NF-kappaB Ligand (RANKL) expression is associated with epithelial to mesenchymal transition in human prostate cancer cells. Cell Res. 2008 Aug;18(8):858-70.

(50.) Poblete CE, Fulla J, Gallardo M, Muñoz V, Castellón EA, Gallegos I, et al. Increased SNAIL expression and low syndecan levels are associated with high Gleason grade in prostate cancer. Int J Oncol. 2014 Mar;44(3):647-54.

(51.) Kalluri R, Neilson EG. Epithelial-mesenchymal transition and its implications for fibrosis. J Clin Invest. 2003 Dec;112(12):1776-84.

(52.) Nelson WJ, Nusse R. Convergence of Wnt, betacatenin, and cadherin pathways. Science. 2004 Mar;303(5663):1483-7.

(53.) Thiery JP, Sleeman JP. Complex networks orchestrate epithelial-mesenchymal transitions. Nat Rev Mol Cell Biol. 2006 Feb;7(2):131-42.

(54.) Gottardi CJ, Wong E, Gumbiner BM. E-cadherin suppresses cellular transformation by inhibiting betacatenin signaling in an adhesion-independent manner. J Cell Biol. 2001 May;153(5):1049-60.

(55.) Thiery JP. Epithelial-mesenchymal transitions in tumour progression. Nat Rev Cancer. 2002 Jun;2(6):442-54.

(56.) Kim K, Lu Z, Hay ED. Direct evidence for a role of beta-catenin/LEF-1 signaling pathway in induction of EMT. Cell Biol Int. 2002;26(5):463-76.

(57.) Yang F, Li X, Sharma M, Sasaki CY, Longo DL, Lim B, et al. Linking beta-catenin to androgen-signaling pathway. J Biol Chem. 2002 Mar;277(13):11336-44.

(58.) Schweizer L, Rizzo CA, Spires TE, Platero JS, Wu Q, Lin TA, et al. The androgen receptor can signal through Wnt/beta-Catenin in prostate cancer cells as an adaptation mechanism to castration levels of an-drogens. BMC Cell Biol. 2008 Jan;9:4.

(59.) Gupta S, Iljin K, Sara H, Mpindi JP, Mirtti T, Vainio P, et al. FZD4 as a mediator of ERG oncogene-induced WNT signaling and epithelial-to-mesenchymal transi-tion in human prostate cancer cells. Cancer Res. 2010 Sep;70(17):6735-45.

(60.) Fuxe J, Vincent T, Garcia de Herreros A. Transcriptional crosstalk between TGF-β and stem cell pathways in tumor cell invasion: role of EMT promoting Smad complexes. Cell Cycle. 2010 Jun;9(12):2363-74.

(61.) Wu CY, Tsai YP, Wu MZ, Teng SC, Wu KJ. Epigenetic reprogramming and post-transcriptional regulation during the epithelial-mesenchymal transition. Trends Genet. 2012 Sep;28(9):454-63.

(62.) Moes M, Le Béchec A, Crespo I, Laurini C, Halava-tyi A, Vetter G, et al. A novel network integrating a miRNA-203/SNAI1 feedback loop which regulates epithelial to mesenchymal transition. PLoS One. 2012;7(4):e35440.

(63.) Xie D, Gore C, Liu J, Pong RC, Mason R, Hao G, et al. Role of DAB2IP in modulating epithelial-to-mes-enchymal transition and prostate cancer metastasis. Proc Natl Acad Sci U S A. 2010 Feb;107(6):2485-90.

(64.) Jing Y, Han Z, Zhang S, Liu Y, Wei L. Epithelial-Mesenchymal Transition in tumor microenvironment. Cell Biosci. 2011 Aug;1:29.

(65.) Marie-Egyptienne DT, Lohse I, Hill RP. Cancer stem cells, the epithelial to mesenchymal transition (EMT) and radioresistance: potential role of hypoxia. Cancer Lett. 2013 Nov;341(1):63-72.

(66.) Zhang J, Ma L. MicroRNA control of epithelial-mesenchymal transition and metastasis. Cancer Metastasis Rev. 2012 Dec;31(3-4):653-62.

(67.) Ru P, Steele R, Newhall P, Phillips NJ, Toth K, Ray RB. miRNA-29b suppresses prostate cancer metastasis by regulating epithelial-mesenchymal transition signaling. Mol Cancer Ther. 2012 May;11(5):1166-73.

(68.) Peng X, Guo W, Liu T, Wang X, Tu X, Xiong D, et al. Identification of miRs-143 and -145 that is associated with bone metastasis of prostate cancer and involved in the regulation of EMT. PLoS One. 2011;6(5):e20341.

(69.) Saini S, Majid S, Yamamura S, Tabatabai L, Suh SO, Shahryari V, et al. Regulatory Role of mir-203 in Pros-tate Cancer Progression and Metastasis. Clin Cancer Res. 2011 Aug;17(16):5287-98.

(70.) Liu Y, Chen XG, Liang CZ. [Expressions of E-cadherin and N-cadherin in prostate cancer and their implica-tions]. Zhonghua Nan Ke Xue. 2014 Sep;20(9):781-6. Chinese.

(71.) Isebaert S, Haustermans K, Van den Bergh L, Joniau S, Dirix P, Oyen R, et al. Identification and characterization of nodal metastases in prostate cancer patients at high risk for lymph node involvement. Acta Oncol. 2013 Oct;52(7):1336-44.

(72.) Liu GL, Yang HJ, Liu T, Lin YZ. Expression and sig-nificance of E-cadherin, N-cadherin, transforming growth factor-β1 and Twist in prostate cancer. Asian Pac J Trop Med. 2014 Jan;7(1):76-82.

(73.) Kachroo N, Warren AY, Gnanapragasam VJ. Multi-transcript profiling in archival diagnostic prosta-te cancer needle biopsies to evaluate biomarkers in non-surgically treated men. BMC Cancer. 2014 Sep;14:673.

(74.) Tanaka H, Kono E, Tran CP, Miyazaki H, Yamashiro J, Shimomura T, et al. Monoclonal antibody targe-ting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance. Nat Med. 2010 Dec;16(12):1414-20.

Descargas

Publicado

23-09-2015

Cómo citar

1.
Benedetti I, Reyes N. Transición epitelial-mesenquimal en la progresión del adenocarcinoma prostático. Iatreia [Internet]. 23 de septiembre de 2015 [citado 22 de enero de 2025];28(4):420-33. Disponible en: https://revistas.udea.edu.co/index.php/iatreia/article/view/20574

Número

Sección

Artículos de revisión