La prolactina promueve migración en las células de cáncer de próstata LNCaP
Resumen
Introducción: La prolactina (PRL) es una hormona que participa en el desarrollo normal de la próstata, pero también en el desarrollo de patologías como el cáncer. El principal problema del cáncer de próstata es su capacidad de producir metástasis. Durante la metástasis las células anormales exhiben mayor migración celular comparado con las células normales; por lo tanto, el aumento de la migración celular es el principal mecanismo para que las células cancerígenas hagan metástasis durante el desarrollo del cáncer. Existe poca información acerca de la participación de la PRL en la migración celular, en especial en el cáncer de próstata. Por lo anterior, se evaluó el efecto de la PRL en la migración celular utilizando como modelo de estudio a las células LNCaP. Objetivo: Evaluar si la PRL induce migración en las células LNCaP. Materiales y Métodos: Utilizamos la técnica de “raspado y cicatrización de herida” para evaluar la migración celular. Se cultivaron células LNCaP en placas de 12 pozos hasta confluencia total, se hizo un rasguño a lo largo del eje de cada pozo y posteriormente fueron estimuladas con 0, 5, 10, 25, 50 100, 150 y 200 nM de PRL. La migración de las células dentro del rasguño fue fotografiada a las 48 h. Resultados: La PRL indujo migración en las células LNCaP. Conclusiones: La PRL indujo migración en las células LNCaP, por lo que esta hormona podría tener alguna participación en la metástasis.
Abstract
Introduction: Prolactin (PRL) is a hormone that participates in the normal development of the prostate but also in the development of pathologies such as cancer. The main problem with prostate cancer is its ability to produce metastasis. During metastasis, abnormal cells exhibit increased cell migration compared to normal cells; therefore, increased cell migration is the main mechanism for cancer cells to become metastasized during cancer development. There is little information about the involvement of PRL in cell migration, especially in prostate cancer. Therefore, the effect of PRL on cell migration was evaluated using LNCaP cells as the study model. Objective: To evaluate whether PRL induce migration in LNCaP cells. Materials and methods: We used the "scratch/wound healing" technique to evaluate cell migration. LNCaP cells were grown in 12-well plates to full confluence, a scratch was made along the axis of each well and were subsequently stimulated with 0, 5, 10, 25, 50, 100, 150 and 200 nM PRL. Migration of the cells within the scratch was photographed at 48 h. Results: PRL induced migration in LNCaP cells. Conclusions: PRL induced migration in LNCaP cells, so this hormone could have some involvement in metastasis.
Keywords: PRL; prostate cancer; cell migration; metastasis.
Palabras clave
Texto completo:
PDFReferencias
Bernichtein S, Touraine P, Goffin V. New concepts in prolactin biology. J. Endocrinol 2010 206: 1–11.
Hernandez ME, Miquel M, Pascual LI, Herrera D, Aranda-Abreu G, López L, Rojas F, Toledo R, Manzo J. Temporalidad en el incremento de receptores a prolactina en el hipotalamo de la rata macho durante la conducta sexual. eNeurobiología 2010 1: 1–8.
Hernandez ME, Wilson MJ. The role of prolactin in the evolution of prostate cancer. Open J. Urol. 2012 2: 188–197.
Costello LC, Franklin RB. Effect of prolactin on the prostate. Prostate 1994 24: 162–166.
Sackmann-Sala L, Goffin V. Prolactin-induced prostate tumorigenesis. En: Diakonova M, Recent advances in prolactin research. Springer 2015 221-242.
Crépin A, Bidaux G, Vanden-Abeele F, Dewailly E, Goffin V, Prevarskaya N, Slomianny C. Prolactin stimulates prostate cell proliferation by increasing endoplasmic reticulum content due to SERCA 2b over-expression. Biochem. J. 2007 401: 49–55.
Har̈könen P. Paracrine prolactin may cause prostatic problems. Endocrinology 2003 144: 2266–2268.
Van Coppenolle F, Slomianny C, Carpentier F, Le Bourhis X, Ahidouch A, Croix D, Legrand G, Dewailly E, Fournier S, Cousse H, Authie D, Raynaud JP, Beauvillain JC, Dupouy JP, Prevarskaya N. Effects of hyperprolactinemia on rat prostate growth: evidence of androgeno-dependence. Am. J. Physiol. Endocrinol. Metab. 2001 280: E120–E129.
Leav I, Merk FB, Lee KF, Loda M, Mandoki M, McNeal JE, Ho SM. Prolactin receptor expression in the developing human prostate and in hyperplastic, dysplastic, and neoplastic lesions. Am. J. Pathol. 1999 154: 863–870.
O’Sullivan CC, Bates SE. Targeting prolactin receptor (PRLR) signaling in PRLR-positive breast and prostate cancer. Oncologist 2016 21: 523–526.
Ben-Jonathan N, LaPensee CR, LaPensee EW. What can we learn from rodents about prolactin in humans? Endocr. Rev. 2008 29: 1–41.
Chen H, Nalbantoglu J. Ring cell migration assay identifies distinct effects of extracellular matrix proteins on cancer cell migration. BMC Res. Notes 2014 7: 1–9.
Doyle AD, Petrie RJ, Kutys ML, Yamada KM. Dimensions in cell migration. Curr. Opin. Cell Biol. 2013 25: 642–649.
Han T, Kang D, Ji D, Wang X, Zhan W, Fu M, Xin HB, Wang JB. How does cancer cell metabolism affect tumor migration and invasion? Cell Adhes. Migr. 2013 7: 395–403.
Stefanoska I, Jovanović-Krivokuća M, Vasilijić S, Ćujić D, Vićovac L. Prolactin stimulates cell migration and invasion by human trophoblast in vitro. Placenta 2013 34: 775–783.
Tan D, Chen KE, Khoo T, Walker AM. Prolactin increases survival and migration of ovarian cancer cells: Importance of prolactin receptor type and therapeutic potential of S179D and G129R receptor antagonists. Cancer Lett. 2011 310: 101–108.
Da Silva PL, do Amaral VC, Gabrielli V, Montt MM, Mannella P, Baracat EC, Soares JM, Simoncini T. Prolactin promotes breast cancer cell migration through actin cytoskeleton remodeling. Front. Endocrinol. 2015 6: 1–8.
Boudjadi S, Carrier JC, Beaulieu JF. Integrin α1 subunit is up-regulated in colorectal cancer. Biomark. Res. 2013 1: 16.
Goffin V, Touraine P. The prolactin receptor as a therapeutic target in human diseases: browsing new potential indications. Expert Opin. Ther. Targets 2015 19: 1229–1244.
Wu W, Ginsburg E, Vonderhaar BK, Walker AM. S179D prolactin increases vitamin D receptor and p21 through up-regulation of short 1b prolactin receptor in human prostate cancer cells. Cancer Res. 2005 65: 7509–7515.
Coppenolle FV, Skryma R, Ouadid-Ahidouch H, Slomianny C, Roudbaraki M, Delcourt P, Dewailly E, Humez S, Crépin A, Gourdou I, Djiane J, Bonnal JL, Mauroy B, Prevarskaya N. Prolactin stimulates cell proliferation through a long form of prolactin receptor and K+ channel activation. Biochem. J. 2004 377: 569–578.
Benson CS, Babu SD, Radhakrishna S, Selvamurugan N, Sankar BR. Expression of matrix metalloproteinases in human breast cancer tissues. Dis. Markers 2013 34: 395–405.
Chen P, Parks WC. Role of matrix metalloproteinases in epithelial migration. J. Cell. Biochem. 2009 108: 1233–1243.
González-Ávila G, González A, Delgado J, Gutiérrez-González LH. Participación de las metaloproteasas de matriz en la progresión del cáncer. Rev. del Inst. Nac. Enfermedades Respir. 2009 22: 328–336.
Goto T, Endo T, Henmi H, Kitajima Y, Kiya T, Nishikawa A, Manase K, Sato H, Kudo R. Gonadotropin-releasing hormone agonist has the ability to induce increased matrix metalloproteinase (MMP)-2 and membrane type 1-MMP expression in corpora lutea, and structural luteolysis in rats. J. Endocrinol. 1999 161: 393–402.
Nagafuchi H, Suzuki N, Kaneko A, Asai T, Sakane T. Prolactin locally produced by synovium infiltrating T lymphocytes induces excessive synovial cell functions in patients with rheumatoid arthritis. J. Rheumatol. 1999 26: 1890–900.
DOI: https://doi.org/10.25009/eb.v8i19.2531
Enlaces refback
- No hay ningún enlace refback.
eNeurobiología es una publicación cuatrimestral editada por el Instituto de Investigaciones Cerebrales de la Universidad Veracruzana. Estamos ubicados en Av. Dr. Luis Castelazo Ayala, s/n, colonia Industrial Ánimas, C.P. 91190, Xalapa-Enríquez, Veracruz, México. Teléfono: 8418900 ext. 13062, www.iice.uv.mx; eneurobiologia@uv.mx. Reserva de Derechos al Uso Exclusivo 04-2023-061314100600-102, otorgada por el Instituto Nacional de Derechos de Autor. ISSN: 2007-3054. Esta obra está bajo una Licencia Creative Commons Attribution 4.0 International.