Browsing by Author "González, Pamela"

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    Diabetic concentrations of metformin inhibit platelet-mediated ovarian cancer cell progression
    (2017) Erices, R.; Cubillos, Sofía; Aravena, Raúl; Santoro, Felice; Márquez, Mónica; Orellana Walden, Renán Felipe; Ramírez, Carolina; González, Pamela; Fuenzalida, Patricia; Bravo Castillo, María Loreto; Oliva, Bárbara; Kato Cardemil, Sumie Rode; Ibáñez, Carolina; Brañes, Jorge; Bravo, Erasmo; Alonso, Catalina
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    Extracellular matrix protein signaling promotes multi-step cancer vasculogenic mimicry formation
    (2025) Mingo Orsini, Gabriel Antonio; Valdivia Román, Andrés Felipe; Santander Zambrano, Gema Nicolle; Babbitt Negrete, Nicole Anike; Aldana Villarroel, Varina Isabel; Pradenas Mateluna, Javiera Macarena Guillerm; González, Pamela; Canales Valenzuela, Cristóbal; Toledo, Jorge A.; Ibáñez, Carolina; Nualart, Francisco; Varas-Godoy, Manuel; Gejman, Roger; Roa, Juan Carlos; Ravasio, Andrea; Bertocchi, Cristina; Owen, Gareth Ivor
    Cancer vasculogenic mimicry (VM) is the formation of vasculature structures in the absence of endothelial cells. We previously established an in vitro model that facilitates the formation of a lumen-containing and fluid-conducting tubular structures after 4 days of cancer cell growth on Matrigel. Herein, we mechanistically characterize this model in breast and ovarian cancer cell lines demonstrating distinct phases of VM formation and the dependence of specific extracellular matrix proteins. We report that VM occurs in four distinct stages. Firstly, alignment, migration then clustering delineate the area of the future tubular structure. Secondly, contraction of aligned structures followed by loss of attachment of some cells and cellular blebbing. Thirdly, a phase of mass proliferation followed by the raising of specific areas of the cancer cell mass above the Matrigel (bridge). Finally, the formation of a cell monolayer closes the tubular structure, forms a glycoprotein-rich luminal lining, then elevates the structure. Only later stages of VM require AKT and FAK signaling, as confirmed by chemical inhibition and phosphorylation analysis. We demonstrate that the lining of the tubular lumen is rich in laminin. Furthermore, the presence of Laminin 111 (but not collagen I) is sufficient in the extracellular matrix (Matrigel) for VM to occur and we confirm that integrin β1, but not integrin β3, is required and this protein changes location during the formation process. RNASeq analysis suggests that VM formation principally occurs through post-transcriptional regulation. As VM is associated with poor patient survival VM, an understanding of the mechanism of VM may bring to light novel biomarkers and anticancer targets.
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    Técnica para cultivar y expandir células de cáncer extraídas de fluido ascitico y su exposición a concentraciones específicas de regímenes de quimioterapia (Chile, concesión n° 55061)
    Owen, Gareth Ivor; Bravo Castillo, María Loreto; González, Pamela; Kato Cardemil, Sumie Rode; Cuello F., Mauricio; Orellana Walden, Renán Felipe