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LOBOS GONZALEZ, LORENA DE LOURDES

Preferred name

Main Affiliation

Facultad de Medicina Clínica Alemana Universidad del Desarrollo

llobos@udd.cl

ORCID

0000-0002-4957-9864

Scopus Author ID

28767817600

Now showing 1 - 10 of 20

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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
3
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Nanoscale outer membrane vesicles from Helicobacter pylori alter astrocyte functionality inducing neuronal degeneration
(2023)
LOBOS GONZALEZ, LORENA DE LOURDES
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PALACIOS, E.
;
S.GUERRERO
;
M. KOGAN
;
B. SHAO
16
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Maraviroc/cisplatin combination inhibits gastric cancer tumoroid growth and improves mice survival
(Springer Science and Business Media LLC, 2025-01-18)
Bárbara Mora-Lagos
;
María Elena Reyes
;
LOBOS GONZALEZ, LORENA DE LOURDES
;
Matías del Campo
;
Kurt Buchegger
Gastric cancer (GC) is a significant cancer-related cause of death worldwide. GC’s most used chemotherapeutic regimen is based on platinum drugs such as cisplatin (CDDP). However, CDDP chemoresistance reduces the survival rate of advanced GC. The immune C-C chemokine receptor type 5 (CCR5) have been proposed as a pivotal factor in cancer progression since its blockade has been linked with antineoplastic effects on tumor cell proliferation; nevertheless, its role in the chemoresistance of GC has not been elucidated. This study aimed to determine the effects induced by the CCR5 using Maraviroc (MVC), a highly selective CCR5 antagonist, on CDDP-resistant AGS cells (AGS R-CDDP), tumoroids (<jats:italic>3D</jats:italic> tumor spheroids), and animal models.</jats:p>
3Scopus© Citations 6
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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
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LOBOS GONZALEZ, LORENA DE LOURDES
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.
6Scopus© Citations 17
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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
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Campos, A.
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Burgos, R.
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Huilcaman, R
;
Gonzalez, M. F
2
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Dataset 2 - Lactadherin: From a Well-Known Breast Tumor Marker to a Possible Player in Extracellular Vesicle-Mediated Cancer Progression
(2022)
LOBOS GONZALEZ, LORENA DE LOURDES
;
EDUARDO FELIPE DURÁN JARA
1
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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
<jats:p>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.</jats:p>
8 1Scopus© Citations 26
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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
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LOBOS GONZALEZ, LORENA DE LOURDES
;
Marcelo Kogan
12 1Scopus© Citations 17
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Exposure to the pro-inflammatory prostaglandin E2 disrupts E-cadherin/Caveolin1-mediated tumor suppression to favor Caveolin-1 enhanced migration, invasion and metastasis of melanoma cells
(2022)
LOBOS GONZALEZ, LORENA DE LOURDES
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FARFÁN BECERRA, NICOLE
;
SILVA, V.
2
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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
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Pamela Contreras-Orellana
;
Pablo Lara
;
Sujey Palma
<jats:p> Aim: To track early events during lung metastasis, we labeled cells expressing (B16F10<jats:sub>CAV1</jats:sub>) or lacking CAV1 (B16F10<jats:sub>mock</jats:sub>) 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. </jats:p>
1 1Scopus© Citations 9

LOBOS GONZALEZ, LORENA DE LOURDES

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