Browsing by Author "Villalon, Manuel"

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    ATP-Dependent Biomechanical Properties of Ciliated and Non-Ciliated Cells Measured by Atomic Force Microscopy
    (CELL PRESS, 2016) Droguett, Karla; Navarrete, Camilo; Fuentes, Christian; Rios, Mariana; Villalon, Manuel; Barrera, Nelson
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    LPS increase of ciliary beat frequency in respiratory ciliated cells
    (FEDERATION AMER SOC EXP BIOL, 2013) Veronica Carreno, Daniela; Llados, Carmen; Rios, Mariana; Cohen, Noam; Villalon, Manuel
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    Progesterone promotes focal adhesion formation and migration in breast cancer cells through induction of protease-activated receptor-1
    (BIOSCIENTIFICA LTD, 2012) Diaz, Jorge; Aranda, Evelyn; Henriquez, Soledad; Quezada, Marisol; Espinoza, Estefania; Loreto Bravo, Maria; Oliva, Barbara; Lange, Soledad; Villalon, Manuel; Jones, Marius; Brosens, Jan J.; Kato, Sumie; Cuello, Mauricio A.; Knutson, Todd P.; Lange, Carol A.; Leyton, Lisette; Owen, Gareth I.
    Progesterone and progestins have been demonstrated to enhance breast cancer cell migration, although the mechanisms are still not fully understood. The protease-activated receptors (PARs) are a family of membrane receptors that are activated by serine proteases in the blood coagulation cascade. PAR1 (F2R) has been reported to be involved in cancer cell migration and overexpressed in breast cancer. We herein demonstrate that PAR1 mRNA and protein are upregulated by progesterone treatment of the breast cancer cell lines ZR-75 and T47D. This regulation is dependent on the progesterone receptor (PR) but does not require PR phosphorylation at serine 294 or the PR proline-rich region mPRO. The increase in PAR1 mRNA was transient, being present at 3 h and returning to basal levels at 18 h. The addition of a PAR1-activating peptide (aPAR1) to cells treated with progesterone resulted in an increase in focal adhesion (FA) formation as measured by the cellular levels of phosphorylated FA kinase. The combined but not individual treatment of progesterone and aPAR1 also markedly increased stress fiber formation and the migratory capacity of breast cancer cells. In agreement with in vitro findings, data mining from the Oncomine platform revealed that PAR1 expression was significantly upregulated in PR-positive breast tumors. Our observation that PAR1 expression and signal transduction are modulated by progesterone provides new insight into how the progestin component in hormone therapies increases the risk of breast cancer in postmenopausal women. Journal of Endocrinology (2012) 214, 165-175
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    The oestrogen metabolite 2-methoxyoestradiol alone or in combination with tumour necrosis factor-related apoptosis-inducing ligand mediates apoptosis in cancerous but not healthy cells of the human endometrium
    (BIOSCIENTIFICA LTD, 2007) Kato, Sumie; Sadarangani, Anil; Lange, Soledad; Villalon, Manuel; Branes, Jorge; Brosens, Jan J.; Owen, Gareth I.; Cuello, Mauricio
    Cancers of the reproductive tract account for 12% of all malignancies in women. As previous studies have shown that oestrogen metabolites can cause apoptosis, we characterised the effect of oestrogen and oestrogen metabolites on non-cancerous and cancerous human endometrial cells. Herein, we demonstrate that 2-methoxyoestradiol (2ME), but not 17 beta-oestradiol, induces apoptosis in cancer cell lines and primary cultured tumours; of endometrial origin. In contrast, 2ME had no effect on cell viability of corresponding normal tissue. This ability of 2ME to induce apoptosis does not require oestrogen receptor activation, but is associated with increased entry into the G2/M phases of the cell cycle and the activation of both the intrinsic and the extrinsic apoptotic pathways. The selective behaviour of 2ME on cancerous as opposed to normal tissue may be due to a reduction in 17 beta -hydroxysteroid dehydrogenase type 11 levels in cancer cells and to a differential down-regulation of superoxide dismutase. Furthermore, we demonstrate that pre-treatment with 2ME enhances the sensitivity of reproductive tract cancer cells to the apoptotic drug tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), without the loss in cell viability to normal cells incurred by currently chemotherapeutic drugs. In conclusion, 2ME, alone or in combination with TRAIL, may be an effective treatment for cancers of uterine origin with minimal toxicity to corresponding healthy female reproductive tissue.
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    TRAIL mediates apoptosis in cancerous but not normal primary cultured cells of the human reproductive tract (vol 12, pg 73, 2007)
    (SPRINGER, 2007) Sadarangani, Anil; Kato, Sumie; Espinoza, Natalia; Lange, Soledad; Llados, Carmen; Espinosa, Marisol; Villalon, Manuel; Lipkowitz, Stanley; Cuello, Mauricio; Owen, Gareth I.
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    Tumor necrosis factor alpha modifies the ciliary beat frequency (CBF) of oviductal ciliated through the prostaglandins and the nitric oxide pathway.
    (SOC STUDY REPRODUCTION, 2007) Perez Sepulveda, Alejandra; Carreno, Daniela; Villalon, Manuel