LOBOS GONZALEZ, LORENA DE LOURDES
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LOBOS GONZALEZ, LORENA DE LOURDES
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llobos@udd.cl
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28767817600

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90 Role of microrna-145 in epithelial ovarian cancer

2020 , Carmen Romero , Maritza P Garrido , Ignacio Torres , Andrea Hernandez , Jonas Chnaiderman , Margarita Vega , Alberto Selman , Jessica Preisler , LOBOS GONZALEZ, LORENA DE LOURDES

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Gold nanoparticles as tracking devices to shed light on the role of caveolin-1 in early stages of melanoma metastasis

2018 , Simón Guerrero , Victor Manuel Díaz-García , Pamela Contreras-Orellana , Pablo Lara , Sujey Palma , Fanny Guzman , LOBOS GONZALEZ, LORENA DE LOURDES , Areli Cárdenas , Ximena Rojas-Silva , Luis Muñoz , Lisette Leyton , Marcelo J Kogan , Andrew FG Quest

Aim: To track early events during lung metastasis, we labeled cells expressing (B16F10CAV1) or lacking CAV1 (B16F10mock) with gold nanoparticles conjugated to the peptide TAT (AuNPs-PEG-TAT). Methods: B16F10 expressing or lacking CAV1 were labeled with AuNPs-PEG-TAT. The physicochemical properties and cytotoxicity of these nanoparticles, as well as their effects on migration and invasiveness of B16F10 cells in vitro were evaluated. Ex vivo lung distribution of the labeled cells after tail vein injection into C57BL/6 mice was examined. Results: AuNPs-PEG-TAT did not affect B16F10 viability, migration and invasiveness. The metastatic and tumorigenic capability of the labeled B16F10 was also not modified in comparison to unlabeled B16F10 cells. CAV1 expression favored the retention of B16F10 cells in the lungs of mice 2 h post injection, suggesting CAV1 promoted adherence to endothelial cells and transendothelial migration. Conclusions: We developed a protocol to label B16F10 cells with AuNPs-PEG-TAT that permits subsequent tracking of cells in mice. CAV1 overexpression was found to increase retention and transendothelial migration of B16F10 cells in the lung.

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Caveolin-1-containing extracellular vesicles transport adhesion proteins and promote malignancy in breast cancer cell lines

2018 , America Campos , Carlos Salomon , Rocio Bustos , Jorge Díaz , Samuel Martínez , Veronica Silva , Constanza Reyes , Natalia Díaz-Valdivia , Manuel Varas-Godoy , LOBOS GONZALEZ, LORENA DE LOURDES , Andrew FG Quest

Breast cancer is one of the most frequently diagnosed cancers and the leading cause of cancer-related deaths in women worldwide, whereby mortality is largely attributable to the development of distant metastasis. Caveolin-1 (CAV1) is a multifunctional membrane protein that is typically upregulated in the final stages of cancer and promotes migration and invasion of tumor cells. Elevated levels of CAV1 have been detected in extracellular vesicles (EVs) from advanced cancer patients. EVs are lipid enclosed vesicular structures that contain bioactive proteins, DNA and RNAs, which can be transferred to other cells and promote metastasis. Therefore, we hypothesized that CAV1 containing EVs released from breast cancer cells may enhance migration and invasion of recipient cells. EVs were purified from conditioned media of MDA-MB-231 wild-type (WT), MDA-MB-231 (shCAV1; possessing the plasmid pLKO.1 encoding a ‘small hairpin’ directed against CAV1) and MDA-MB-231 (shC) short hairpin control cells. Nanoparticle tracking analysis revealed an average particle size of 40–350 nm for all preparations. As anticipated, CAV1 was detected in MDA-MB-231 WT and shC EVs, but not in MDA-MB-231 (shCAV1) EVs. Mass spectrometry analysis revealed the presence of specific cell adhesion-related proteins, such as Cyr61, tenascin (TNC) and S100A9 only in WT and shC, but not in shCAV1 EVs. Importantly, EVs containing CAV1 promoted migration and invasion of cells lacking CAV1. We conclude that the presence of CAV1 in EVs from metastatic breast cancer cells is associated with enhanced migration and invasiveness of recipient cells in vitro, suggesting that intercellular communication promoted by EVs containing CAV1 will likely favor metastasis in vivo.

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Gold nanoparticle based double-labeling of melanoma extracellular vesicles to determine the specificity of uptake by cells and preferential accumulation in small metastatic lung tumors

2020 , Pablo Lara , Sujey Palma-Florez , Edison Salas-Huenuleo , Iva Polakovicova , Simón Guerrero , LOBOS GONZALEZ, LORENA DE LOURDES , America Campos , Luis Muñoz , Carla Jorquera-Cordero , Manuel Varas-Godoy , Jorge Cancino , Eloísa Arias , Jaime Villegas , Luis J. Cruz , Fernando Albericio , Eyleen Araya , Alejandro H. Corvalan , Andrew F. G. Quest , Marcelo J. Kogan

Abstract Background Extracellular vesicles (EVs) have shown great potential for targeted therapy, as they have a natural ability to pass through biological barriers and, depending on their origin, can preferentially accumulate at defined sites, including tumors. Analyzing the potential of EVs to target specific cells remains challenging, considering the unspecific binding of lipophilic tracers to other proteins, the limitations of fluorescence for deep tissue imaging and the effect of external labeling strategies on their natural tropism. In this work, we determined the cell-type specific tropism of B16F10-EVs towards cancer cell and metastatic tumors by using fluorescence analysis and quantitative gold labeling measurements. Surface functionalization of plasmonic gold nanoparticles was used to promote indirect labeling of EVs without affecting size distribution, polydispersity, surface charge, protein markers, cell uptake or in vivo biodistribution. Double-labeled EVs with gold and fluorescent dyes were injected into animals developing metastatic lung nodules and analyzed by fluorescence/computer tomography imaging, quantitative neutron activation analysis and gold-enhanced optical microscopy. Results We determined that B16F10 cells preferentially take up their own EVs, when compared with colon adenocarcinoma, macrophage and kidney cell-derived EVs. In addition, we were able to detect the preferential accumulation of B16F10 EVs in small metastatic tumors located in lungs when compared with the rest of the organs, as well as their precise distribution between tumor vessels, alveolus and tumor nodules by histological analysis. Finally, we observed that tumor EVs can be used as effective vectors to increase gold nanoparticle delivery towards metastatic nodules. Conclusions Our findings provide a valuable tool to study the distribution and interaction of EVs in mice and a novel strategy to improve the targeting of gold nanoparticles to cancer cells and metastatic nodules by using the natural properties of malignant EVs.

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Caveolin-1-containing extracellular vesicles transport adhesion proteins which promote the development of malignant traits in recipient cells

2021 , LOBOS GONZALEZ, LORENA DE LOURDES , Campos, A. , Burgos, R. , Huilcaman, R , Gonzalez, M. F , Diaz, J. , Varas, M. , Leyton, L. , Quest, A. F. G.

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Mitochondrial ncRNA targeting induces cell cycle arrest and tumor growth inhibition of MDA-MB-231 breast cancer cells through reduction of key cell cycle progression factors

2019 , Christopher Fitzpatrick , Maximiliano F. Bendek , Macarena Briones , Nicole Farfán , Valeria A. Silva , Gino Nardocci , Martín Montecino , Anne Boland , Jean-François Deleuze , Jaime Villegas , Claudio Villota , Verónica Silva , LOBOS GONZALEZ, LORENA DE LOURDES , Vincenzo Borgna , Eric Barrey , Luis O. Burzio , Verónica A. Burzio

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Inhibition of PORCN Blocks Wnt Signaling to Attenuate Progression of Oral Carcinogenesis

2023 , Daniel Peña-Oyarzún , Tania Flores , Vicente A. Torres , Andrew F.G. Quest , LOBOS GONZALEZ, LORENA DE LOURDES , Catalina Kretschmar , Pamela Contreras , Andrea Maturana-Ramírez , Alfredo Criollo , Montserrat Reyes

Oral squamous cell carcinoma (OSCC) is commonly preceded by potentially malignant lesions, referred to as oral dysplasia. We recently reported that oral dysplasia is associated with aberrant activation of the Wnt/β-catenin pathway, due to overexpression of Wnt ligands in a Porcupine (PORCN)-dependent manner. Pharmacologic inhibition of PORCN precludes Wnt secretion and has been proposed as a potential therapeutic approach to treat established cancers. Nevertheless, there are no studies that explore the effects of PORCN inhibition at the different stages of oral carcinogenesis.

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Pannexin-1 expression in tumor cells correlates with colon cancer progression and survival

2024 , Aaron Fierro-Arenas , Glauben Landskron , Ilan Camhi-Vainroj , Benjamín Basterrechea , Daniela Parada-Venegas , LOBOS GONZALEZ, LORENA DE LOURDES , Karen Dubois-Camacho , Catalina Araneda , Camila Romero , Antonia Domínguez , Gonzalo Vásquez , Francisco López-K , Karin Alvarez , Carlos M. González , Carolina Hager Ribeiro , Elisa Balboa , Eliseo Eugenin , Marcela A. Hermoso , Marjorie De la Fuente López

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Biomimetic quantum dot-labeled B16F10 murine melanoma cells as a tool to monitor early steps of lung metastasis by in vivo imaging

2018 , Victor Manuel Díaz-García , Simón Guerrero , Natalia Díaz-Valdivia , LOBOS GONZALEZ, LORENA DE LOURDES , Marcelo Kogan , José Pérez-Donoso , Andrew F.G. Quest

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Coagulation Factor Xa Promotes Solid Tumor Growth, Experimental Metastasis and Endothelial Cell Activation

2019 , Maximiliano Arce , Mauricio P. Pinto , Macarena Galleguillos , Catalina Muñoz , Soledad Lange , Carolina Ramirez , Rafaela Erices , Pamela Gonzalez , Ethel Velasquez , Fabián Tempio , Mercedes N. Lopez , Flavio Salazar-Onfray , Kelly Cautivo , Alexis M. Kalergis , Sebastián Cruz , Álvaro Lladser , LOBOS GONZALEZ, LORENA DE LOURDES , Guillermo Valenzuela , Nixa Olivares , Claudia Sáez , Tania Koning , Fabiola A. Sánchez , Patricia Fuenzalida , Alejandro Godoy , Pamela Contreras Orellana , Lisette Leyton , Roberta Lugano , Anna Dimberg , Andrew F.G. Quest , Gareth I. Owen

Hypercoagulable state is linked to cancer progression; however, the precise role of the coagulation cascade is poorly described. Herein, we examined the contribution of a hypercoagulative state through the administration of intravenous Coagulation Factor Xa (FXa), on the growth of solid human tumors and the experimental metastasis of the B16F10 melanoma in mouse models. FXa increased solid tumor volume and lung, liver, kidney and lymph node metastasis of tail-vein injected B16F10 cells. Concentrating on the metastasis model, upon coadministration of the anticoagulant Dalteparin, lung metastasis was significantly reduced, and no metastasis was observed in other organs. FXa did not directly alter proliferation, migration or invasion of cancer cells in vitro. Alternatively, FXa upon endothelial cells promoted cytoskeleton contraction, disrupted membrane VE-Cadherin pattern, heightened endothelial-hyperpermeability, increased inflammatory adhesion molecules and enhanced B16F10 adhesion under flow conditions. Microarray analysis of endothelial cells treated with FXa demonstrated elevated expression of inflammatory transcripts. Accordingly, FXa treatment increased immune cell infiltration in mouse lungs, an effect reduced by dalteparin. Taken together, our results suggest that FXa increases B16F10 metastasis via endothelial cell activation and enhanced cancer cell-endothelium adhesion advocating that the coagulation system is not merely a bystander in the process of cancer metastasis.

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