Artículos relacionadosArtículos relacionadosArtículos relacionados
Artículos afines de siicsalud publicados en los últimos 4 meses
EFECTOS DE LAS VITAMINAS ANTIOXIDANTES EN LA ENDOMETRIOSIS
Reproductive Biology and Endocrinology Rb&e 21(1):1-16
Difundido en siicsalud: 4 sep 2024
TRABAJO DE PARTO INDUCIDO: LONGITUD CERVICAL COMO PREDICTOR DE ÉXITO
Ginecología y Obstetricia de México 92(6):224-236
Difundido en siicsalud: 24 sep 2024

DEFICIENCIA DE RETINOIDES Y CONSUMO DE ESTROGENOS COMO COFACTORES DE RIESGO EN EL CANCER CERVICAL

(especial para SIIC © Derechos reservados)
Estudiar el papel que desempeñan algunos factores de riesgo en el desarrollo del cáncer cervicouterino. La infección con papilomavirus (HPV) de alto riesgo, el uso de anticonceptivos orales y una dieta deficiente de Retinoides, son factores de riesgo que inducen eventos genéticos o epigenéticos en cáncer cervical.
gariglio9.jpg Autor:
Patricio Gariglio
Columnista Experto de SIIC

Institución:
CINVESTAV


Artículos publicados por Patricio Gariglio
Coautor
E Rios* 
Bióloga, CINVESTAV, Distrito Federal, México*
Recepción del artículo
13 de Julio, 2012
Aprobación
2 de Octubre, 2012
Primera edición
11 de Octubre, 2012
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La infección persistente por el virus del papiloma humano de alto riesgo (HR-HPV) está relacionada con la aparición de cáncer cervical (CC), una de las principales causas de mortalidad por cáncer en todo el mundo. La infección se produce en la zona de transformación, la región más sensible del cérvix a estrógenos y retinoides. El CC afecta a un bajo porcentaje de mujeres infectadas por HR-HPV y tarda en desarrollarse hasta décadas después de la infección, lo que sugiere que el HR-HPV es necesario pero no suficiente para causar CC. Otros factores son necesarios para la progresión desde la infección por HR-HPV hasta el cáncer, como por ejemplo: uso de anticonceptivos orales por largos períodos, fumar, partos múltiples, falta de micronutrientes, particularmente una dieta baja en retinoides, los cuales alteran la diferenciación epitelial, el crecimiento celular y la apoptosis de las células malignas. La detección precoz del HR-HPV y el manejo de lesiones precancerosas, aunado a un conocimiento detallado de factores de riesgo adicionales, puede ser una estrategia para prevenir esta enfermedad. La presente revisión se enfoca en explicar el efecto de los estrógenos, la deficiencia de retinoides y el HR-HPV en la aparición del CC. Dichos cofactores pueden actuar en conjunto para inducir transformación neoplásica en el epitelio escamoso del cérvix, promoviendo un segundo evento genético o epigenético que lleve a la aparición del CC.

Palabras clave
estrógenos, retinoides, papilomavirus, cáncer cervical, RAR


Artículo completo

(castellano)
Extensión:  +/-8.95 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
Persistent infection with high-risk human papillomaviruses (HR-HPVs) is involved in cervical cancer (CC), a major cause of cancer mortality worldwide. Infection occurs primarily at the transformation zone (TZ), the most estrogen- and retinoid-sensitive region of the cervix. Development of CC affects a small percentage of HR-HPV-infected women and often takes decades after infection, suggesting that HR-HPV is a necessary but not sufficient cause of CC. Thus, other cofactors are necessary for progression from cervical HR-HPV infection to cancer such as long-term use of hormonal contraceptives, multiparity, smoking, as well as micronutrient depletion and in particular retinoid deficiency, which alters epithelial differentiation, cellular growth and apoptosis of malignant cells. Therefore, early detection of HR-HPV and management of precancerous lesions together with a profound understanding of additional risk factors could be a strategy to avoid this disease. In this review we focus on the synergic effect of estrogens, retinoid deficiency and HR-HPVs in the development of CC. These risk factors may act in concert to induce neoplastic transformation in the squamous epithelium of the cervix, setting the stage for secondary genetic or epigenetic events leading to cervical cancer.

Key words
estrogens, retinoids, papillomavirus, cervical cáncer, RAR


Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Anatomía Patológica, Obstetricia y Ginecología
Relacionadas: Bioquímica, Diagnóstico por Laboratorio, Endocrinología y Metabolismo, Oncología



Comprar este artículo
Extensión: 8.95 páginas impresas en papel A4

file05.gif (1491 bytes) Artículos seleccionados para su compra



Enviar correspondencia a:
Patricio Gariglio, Centro de Investigación y de Estudios Avanzados del IPN, C.P. 07360, Av. Instituto Politécnico Nacional No. 2508 Col. San Pedro , México, D.F., Zacatenco, México
Bibliografía del artículo
1. Walboomers JM, Jacobs MV, Manos MM, y col. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol. 189(1):12-9, 1999.

2. Brown DR, Schroeder JM, Bryan JT, Stoler MH, Fife KH. Detection of multiple human papillomavirus types in Condylomata acuminata lesions from otherwise healthy and immunosuppressed patients. J Clin Microbiol. (10):3316-22, 1999.

3. Li N, Franceschi S, Howell-Jones R, Snijders PJ, Clifford GM. Human papillomavirus type distribution in 30,848 invasive cervical cancers worldwide: Variation by geographical region, histological type and year of publication. Int J Cancer. 128(4):927-35, 2011.

4. Burk RD, Chen Z, Van Doorslaer K. Human papillomaviruses: genetic basis of carcinogenicity. Public Health Genomics. 12(5-6):281-90, 2009.

5. Thierry F. Transcriptional regulation of the papillomavirus oncogenes by cellular and viral transcription factors in cervical carcinoma. Virology. 384(2):375-9, 2009.

6. Pim D, Banks L. Interaction of viral oncoproteins with cellular target molecules: infection with high-risk vs low-risk human papillomaviruses. APMIS. 118(6-7):471-93, 2010.

7. Bromberg-White JL, Meyers C. Comparison of the basal and glucocorticoid-inducible activities of the upstream regulatory regions of HPV18 and HPV31 in multiple epithelial cell lines. Virology. 306(2):197-202, 2003.

8. McLaughlin-Drubin ME, Münger K. The human papillomavirus E7 oncoprotein. Virology. 384(2):335-44, 2009.

9. Ghittoni R, Accardi R, Hasan U, Gheit T, Sylla B, Tommasino M. The biological properties of E6 and E7 oncoproteins from human papillomaviruses. Virus Genes. 40(1):1-13, 2010.

10. Zheng J, Vaheri A. Human epithelial cells immortalized by human papilloma viruses. Crit Rev Oncog. 6(3-6):235-50, 1995.

11. Lagunas-Martínez A, Madrid-Marina V, Gariglio P. Modulation of apoptosis by early human papillomavirus proteins in cervical cancer. Biochim Biophys Acta. 1805(1):6-16, 2010.

12. Javier RT. Cell polarity proteins: common targets for tumorigenic human viruses. Oncogene. 27(55):7031-46, 2008.

13. Yan X, Shah W, Jing L, Chen H, Wang Y. High-risk human papillomavirus type 18 E7 caused p27 elevation and cytoplasmic localization. Cancer Biol Ther. 9(9):728-35, 2010.

14. Kim YT, Zhao M. Aberrant cell cycle regulation in cervical carcinoma. Yonsei Med J. 46(5):597-613, 2005.

15. Severino A, Abbruzzese C, Manente L, y col. Human papillomavirus-16 E7 interacts with Siva-1 and modulates apoptosis in HaCaT human immortalized keratinocytes. J Cell Physiol. 212(1):118-25, 2007.

16. Mammas IN, Sourvinos G, Giannoudis A, Spandidos DA. Human papilloma virus (HPV) and host cellular interactions. Pathol Oncol Res. 14(4):345-54, 2008.

17. Bosch FX, Lorincz A, Muñoz N, Meijer CJ, Shah KV. The causal relation between human papillomavirus and cervical cancer. J Clin Pathol. 55(4):244-65, 2002.

18. Castellsagué X, Muñoz N. Chapter 3: Cofactors in human papillomavirus carcinogenesis--role of parity, oral contraceptives, and tobacco smoking. J Natl Cancer Inst Monogr. (31):20-8, 2003.

19. Gadducci A, Barsotti C, Cosio S, Domenici L, Riccardo Genazzani A. Smoking habit, immune suppression, oral contraceptive use, and hormone replacement therapy use and cervical carcinogenesis: a review of the literature. Gynecol Endocrinol. 27(8):597-604, 2011.

20. Chuang LC, Hu CY, Chen HC, y col. Associations of human leukocyte antigen class II genotypes with human papillomavirus 18 infection and cervical intraepithelial neoplasia risk. Cancer. 2011.

21. Doorbar J. Molecular biology of human papillomavirus infection and cervical cancer. Clin Sci (Lond). 110(5):525-41, 2006.

22. Muñoz N, Franceschi S, Bosetti C, y col. Multicentric Cervical Cancer Study Group. Role of parity and human papillomavirus in cervical cancer: the IARC multicentric case-control study. Lancet. 359(9312):1093-101, 2002.

23. Singh M, Singh N. Curcumin counteracts the proliferative effect of estradiol and induces apoptosis in cervical cancer cells. Mol Cell Biochem. 347(1-2):1-11, 2011.

24. Piyathilake CJ. Update on micronutrients and cervical dysplasia. Ethn Dis. 17(2 Suppl 2):S2-14-7, 2007.

25. Peterson CE, Sedjo RL, Davis FG, Beam CA, Giuliano AR. Combined antioxidant carotenoids and the risk of persistent human papillomavirus infection. Nutr Cancer. 62(6):728-33, 2010.

26. Goodman M, Bostick RM, Kucuk O, Jones DP. Clinical trials of antioxidants as cancer prevention agents: Past, present, and future. Free Radic Biol Med. 51(5):1068-84, 2011.

27. Chatterjee M, Janarthan M, Chatterjee M. Biological Activity of Carotenoids: its Implications in Cancer Risk and Prevention. Curr Pharm Biotechnol, 2011.

28. Giannoni E, Parri M, Chiarugi P. EMT and Oxidative Stress: A Bidirectional Interplay Affecting Tumor Malignancy. Antioxid Redox Signal. 2011.

29. Ghosh C, Baker JA, Moysich KB, Rivera R, Brasure JR, McCann SE. Dietary intakes of selected nutrients and food groups and risk of cervical cancer. Nutr Cancer. 60(3):331-41, 2008.

30. Cavell BE, Syed Alwi SS, Donlevy A, Packham G. Anti-angiogenic effects of dietary isothiocyanates: mechanisms of action and implications for human health. Biochem Pharmacol. 81(3):327-36, 2011.

31. Sepkovic DW, Bradlow HL. Estrogen hydroxylation--the good and the bad. Ann N Y Acad Sci. 1155:57-67, 2009.

32. Vicent GP, Nacht AS, Zaurín R, Ballaré C, Clausell J, Beato M. Minireview: role of kinases and chromatin remodeling in progesterone signaling to chromatin. Mol Endocrinol. 24(11):2088-98, 2010.

33. Kurita T. Normal and abnormal epithelial differentiation in the female reproductive tract. Differentiation. 82(3):117-26, 2011.

34. Chung SH, Wiedmeyer K, Shai A, Korach KS, Lambert PF. Requirement for estrogen receptor alpha in a mouse model for human papillomavirus-associated cervical cancer. Cancer Res. 68(23):9928-34, 2008.

35. Delvenne P, Herman L, Kholod N, y col. Role of hormone cofactors in the human papillomavirus-induced carcinogenesis of the uterine cervix. Mol Cell Endocrinol. 264(1-2):1-5, 2007.

36. Nair HB, Luthra R, Kirma N, y col. Induction of aromatase expression in cervical carcinomas: effects of endogenous estrogen on cervical cancer cell proliferation. Cancer Res. 65(23):11164-73, 2005.

37. Zhao C, Dahlman-Wright K, Gustafsson JÅ. Estrogen signaling via estrogen receptor {beta}. J Biol Chem. 285(51):39575-9, 2010.

38. Kang L, Zhang X, Xie Y, y col. Involvement of estrogen receptor variant ER-alpha36, not GPR30, in nongenomic estrogen signaling. Mol Endocrinol. 24(4):709-21, 2010.

39. Martin LA, Farmer I, Johnston SR, Ali S, Dowsett M. Elevated ERK1/ERK2/estrogen receptor cross-talk enhances estrogen-mediated signaling during long-term estrogen deprivation. Endocr Relat Cancer. 12 Suppl 1:S75-84, 2005.

40. Song S, Pitot HC, Lambert PF. The human papillomavirus type 16 E6 gene alone is sufficient to induce carcinomas in transgenic animals. J Virol. 73(7):5887-93, 1999.
41. Herber R, Liem A, Pitot H, Lambert PF. Squamous epithelial hyperplasia and carcinoma in mice transgenic for the human papillomavirus type 16 E7 oncogene. J Virol. 70(3):1873-81, 1996.

42. Song S, Liem A, Miller JA, Lambert PF. Human papillomavirus types 16 E6 and E7 contribute differently to carcinogenesis. Virology. 267(2):141-50, 2000.

43. Arbeit JM, Howley PM, Hanahan D. Chronic estrogen-induced cervical and vaginal squamous carcinogenesis in human papillomavirus type 16 transgenic mice. Proc Natl Acad Sci U S A. 93(7):2930-5, 1996.

44. Elson DA, Riley RR, Lacey A, Thordarson G, Talamantes FJ, Arbeit JM. Sensitivity of the cervical transformation zone to estrogen-induced squamous carcinogenesis. Cancer Res. 60(5):1267-75, 2000.

45. Riley RR, Duensing S, Brake T, Münger K, Lambert PF, Arbeit JM. Dissection of human papillomavirus E6 and E7 function in transgenic mouse models of cervical carcinogenesis. Cancer Res. 63(16):4862-71, 2003.

46. Brake T, Lambert PF. Estrogen contributes to the onset, persistence, and malignant progression of cervical cancer in a human papillomavirus-transgenic mouse model. Proc Natl Acad Sci U S A. 102(7):2490-5, 2005.

47. Shai A, Brake T, Somoza C, Lambert PF. The human papillomavirus E6 oncogene dysregulates the cell cycle and contributes to cervical carcinogenesis through two independent activities. Cancer Res. 67(4):1626-35, 2007.

48. Park JS, Rhyu JW, Kim CJ, y col. Neoplastic change of squamo-columnar junction in uterine cervix and vaginal epithelium by exogenous estrogen in hpv-18 URR E6/E7 transgenic mice. Gynecol Oncol. 89(3):360-8, 2007.

49. Schneider C, Jick SS, Meier CR. Risk of gynecological cancers in users of estradiol/dydrogesterone or other HRT preparations. Climacteric. 12(6):514-24, 2009.

50. Salazar EL, Sojo-Aranda I, López R, Salcedo M. The evidence for an etiological relationship between oral contraceptive use and dysplastic change in cervical tissue. Gynecol Endocrinol. 15(1):23-8, 2001.

51. de Villiers EM. Relationship between steroid hormone contraceptives and HPV, cervical intraepithelial neoplasia and cervical carcinoma. Int J Cancer. 103(6):705-8, 2003.

52. Tjalma WA, Van Waes TR, Van den Eeden LE, Bogers JJ. Role of human papillomavirus in the carcinogenesis of squamous cell carcinoma and adenocarcinoma of the cervix. Best Pract Res Clin Obstet Gynaecol. 19(4):469-83, 2005.

53. Piersma SJ. Immunosuppressive Tumor Microenvironment in Cervical Cancer Patients. Cancer Microenviron. 2011.

54. Kaushic C, Frauendorf E, Rossoll RM, Richardson JM, Wira CR. Influence of the estrous cycle on the presence and distribution of immune cells in the rat reproductive tract. Am J Reprod Immunol. 39(3):209-16, 1998.

55. Wira CR, Grant-Tschudy KS, Crane-Godreau MA. Epithelial cells in the female reproductive tract: a central role as sentinels of immune protection. Am J Reprod Immunol. 53(2):65-76, 2005.

56. Helm CW, Lorenz DJ, Meyer NJ, Rising WR, Wulff JL. Retinoids for preventing the progression of cervical intra-epithelial neoplasia. Cochrane Database Syst Rev. (4):CD003296, 2007.

57. Gariglio P, Gutiérrez J, Cortés E, Vázquez J. The role of retinoid deficiency and estrogens as cofactors in cervical cancer. Arch Med Res. 40(6):449-65, 2009.

58. Pérez E, Bourguet W, Gronemeyer H, de Lera AR. Modulation of RXR function through ligand design. Biochim Biophys Acta. 2011.

59. Flajollet S, Lefebvre B, Rachez C, Lefebvre P. Distinct roles of the steroid receptor coactivator 1 and of MED1 in retinoid-induced transcription and cellular differentiation. J Biol Chem. 281(29):20338-48, 2006.
60. O'Malley BW, Kumar R. Nuclear receptor coregulators in cancer biology. Cancer Res. 69(21):8217-22, 2009.

61. Han SJ, Lonard DM, O'Malley BW. Multi-modulation of nuclear receptor coactivators through posttranslational modifications. Trends Endocrinol Metab. 20(1):8-15, 2009.

62. Kato S, Fujiki R. Transcriptional controls by nuclear fat-soluble vitamin receptors through chromatin reorganization. Biosci Biotechnol Biochem. 75(3):410-3, 2011.

63. Darwiche N, Celli G, De Luca LM. Specificity of retinoid receptor gene expression in mouse cervical epithelia. Endocrinology. 134(5):2018-25, 1994.

64. Ocadiz-Delgado R, Castaneda-Saucedo E, Indra AK, Hernandez-Pando R, Gariglio P. Impaired cervical homeostasis upon selective ablation of RXRalpha in epithelial cells. Genesis. 46(1):19-28, 2008.

65. Ocadiz-Delgado R, Castañeda-Saucedo E, Indra AK, y col. RXRa deletion and E6E7 oncogene expression are sufficient to induce cervical malignant lesions in vivo. Cancer Lett. 2011.

66. Chambon P. A decade of molecular biology of retinoic acid receptors. FASEB J. 10(9):940-54, 1996.

67. Xu XC. Tumor-suppressive activity of retinoic acid receptor-beta in cancer. Cancer Lett. 253(1):14-24, 2007.

68. Nagpal S, Zelent A, Chambon P. RAR-beta 4, a retinoic acid receptor isoform is generated from RAR-beta 2 by alternative splicing and usage of a CUG initiator codon. Proc Natl Acad Sci U S A. 89(7):2718-22, 1992.

69. Abu J, Batuwangala M, Symonds P. Expression of RAR beta2 gene by real-time RT-PCR: differential expression in normal subjects compared to cervical cancer patients normalised against GAPDH as a housekeeping gene. Eur J Obstet Gynecol Reprod Biol. 140(2):295-6, 2008.

70. Tang XH, Gudas LJ. Retinoids, retinoic acid receptors, and cancer. Annu Rev. Pathol. 6:345-64, 2011.

71. Geisen C, Denk C, Gremm B, y col. High-level expression of the retinoic acid receptor beta gene in normal cells of the uterine cervix is regulated by the retinoic acid receptor alpha and is abnormally down-regulated in cervical carcinoma cells. Cancer Res. 57(8):1460-7, 1997.

72. Shimizu M, Suzui M, Deguchi A, Lim JT, Weinstein IB. Effects of acyclic retinoid on growth, cell cycle control, epidermal growth factor receptor signaling, and gene expression in human squamous cell carcinoma cells. Clin Cancer Res. 10(3):1130-40, 2004.

73. Altucci L, Leibowitz MD, Ogilvie KM, de Lera AR, Gronemeyer H. RAR and RXR modulation in cancer and metabolic disease. Nat Rev Drug Discov. 6(10):793-810, 2007.

74. Park SH, Lim JS, Jang KL. All-trans retinoic acid induces cellular senescence via upregulation of p16, p21, and p27. Cancer Lett. 310(2):232-9, 2011.

75. Ma Y, Feng Q, Sekula D, Diehl JA, Freemantle SJ, Dmitrovsky E. Retinoid targeting of different D-type cyclins through distinct chemopreventive mechanisms. Cancer Res. 65(14):6476-83, 2005.

76. Luo P, Lin M, Lin M, Chen Y, Yang B, He Q. Function of retinoid acid receptor alpha and p21 in all-trans-retinoic acid-induced acute T-lymphoblastic leukemia apoptosis. Leuk Lymphoma. 50(7):1183-9, 2009.

77. Sah JF, Eckert RL, Chandraratna RA, Rorke EA. Retinoids suppress epidermal growth factor-associated cell proliferation by inhibiting epidermal growth factor receptor-dependent ERK1/2 activation. J Biol Chem. 277(12):9728-35, 2002.

78. Dhandapani L, Yue P, Ramalingam SS, Khuri FR, Sun SY. Retinoic acid enhances TRAIL-induced apoptosis in cancer cells by upregulating TRAIL receptor 1 expression. Cancer Res. 71(15):5245-54, 2011.

79. Haque A, Banik NL, Ray SK. Emerging role of combination of all-trans retinoic acid and interferon-gamma as chemoimmunotherapy in the management of humanglioblastoma. Neurochem Res. 32(12):2203-9, 2007.

80. Kalvakolanu DV, Nallar SC, Kalakonda S. Cytokine-induced tumor suppressors: a GRIM story. Cytokine. 52(1-2):128-42, 2010.

81. Alvarez S, Bourguet W, Gronemeyer H, de Lera AR. Retinoic acid receptor modulators: a perspective on recent advances and promises. Expert Opin Ther Pat. 21(1):55-63, 2011.

82. Okuno M, Kojima S, Matsushima-Nishiwaki R, y col. Retinoids in cancer chemoprevention. Curr Cancer Drug Targets. 4(3):285-98, 2004.

83. Kurie JM, Lotan R, Lee JJ, y col. Treatment of former smokers with 9-cis-retinoic acid reverses loss of retinoic acid receptor-beta expression in the bronchial epithelium: results from a randomized placebo-controlled trial. J Natl Cancer Inst. 95(3):206-14, 2003.

84. Mongan NP, Gudas LJ. Valproic acid, in combination with all-trans retinoic acid and 5-aza-2'-deoxycytidine, restores expression of silenced RARbeta2 in breast cancer cells. Mol Cancer Ther. 4(3):477-86, 2005.

85. Jiang W, Deng W, Bailey SK, y col. Prevention of KLF4-mediated tumor initiation and malignant transformation by UAB30 rexinoid. Cancer Biol Ther. 8(3):289-98, 2009.

86. Kashyap V, Rezende NC, Scotland KB, y col. Regulation of stem cell pluripotency and differentiation involves a mutual regulatory circuit of the NANOG, OCT4, and SOX2 pluripotency transcription factors with polycomb repressive complexes and stem cell microRNAs. Stem Cells Dev. 18(7):1093-108, 2009.

 
 
 
 
 
 
 
 
 
 
 
 
Está expresamente prohibida la redistribución y la redifusión de todo o parte de los contenidos de la Sociedad Iberoamericana de Información Científica (SIIC) S.A. sin previo y expreso consentimiento de SIIC.
Artículos relacionadosMás relacionadosAtículos relacionados
PROFILAXIS ADYUVANTE CON AZITROMICINA EN EL MOMENTO DE LA CESÁREA NO ELECTIVA
The Journal of Maternal Fetal & Neonatal Medicine 37(1):1-5
Difundido en siicsalud: 24 sep 2024
RADIOTERAPIA DEFINITIVA Y CONTROL LOCAL DEL CÁNCER DE VAGINA
BMC Cancer 24(707):1-10
Difundido en siicsalud: 2 jul 2024
ua31618