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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2023 2023 2022 2022 2021 2021 2020 2020 2019 2019 2018 2018 0.0 0.0 0.2 0.2 0.4 0.4 0.6 0.6 0.8 0.8 1.0 1.0

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Publication

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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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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