Publications by authors named "Belen Mezquita"
Aim: To describe the use of bibliometrics in nursing and assess their contribution to research and practice.
Design: A content analysis was conducted of topics, data sources and applications of bibliometrics in nursing research articles.
Methods: The study universe included 129 bibliometric articles on nursing retrieved from Scopus.
Stem cells have the capacity of self-renewal and, through proliferation and differentiation, are responsible for the embryonic development, postnatal development, and the regeneration of tissues in the adult organism. Cancer stem cells, analogous to the physiological stem cells, have the capacity of self-renewal and may account for growth and recurrence of tumors. Development and regeneration of healthy tissues and tumors depend on the balance of different genomic and nongenomic signaling pathways that regulate stem cell quiescence, proliferation, and differentiation.
View Article and Find Full Text PDFAll-trans-retinoic acid (RA), the active metabolite of vitamin A, can reduce the malignant phenotype in some types of cancer and paradoxically also can promote cancer growth and invasion in others. For instance, it has been reported that RA induces tumor suppression in tumor xenografts of MDA-MB-468 breast cancer cells while increasing tumor growth and metastases in xenografts of MDA-MB-231 breast cancer cells. The signaling pathways involved in the pro-invasive action of retinoic acid remain mostly unknown.
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- Oxaliplatin-resistant LoVo colon cancer cells show increased c-MET and VEGFR-1 expression compared to chemosensitive cells, but surprisingly have reduced VEGF levels.
- These resistant cells also activate additional signaling pathways related to chemoresistance, including Akt and β-catenin-TCF4, while the phosphorylation of c-MET is decreased when VEGF is introduced into their environment.
- VEGF inhibits c-MET phosphorylation through VEGFR-1, and when VEGFR-1 is silenced, the phosphorylation of c-MET is restored, indicating a complex interaction that may impact the effectiveness of anti-VEGF therapies in tumors expressing both receptors.
Type 1 diabetes is an autoimmune condition caused by the lymphocyte-mediated destruction of the insulin-producing β cells in pancreatic islets. We aimed to identify final molecular entities targeted by the autoimmune assault on pancreatic β cells that are causally related to β cell viability. Here, we show that cyclin D3 is targeted by the autoimmune attack on pancreatic β cells in vivo.
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- Src activation is crucial in cancer development, with just five minutes being enough for transformation and cancer stem cell maintenance.
- Various tyrosine kinase receptors play a key role in activating Src through ligand binding, while some intracellular receptor isoforms can activate Src without this binding.
- The i21-VEGFR-1 isoform in breast cancer cells can upregulate Src activation via the Notch signaling pathway, suggesting potential therapeutic strategies using Notch inhibitors and retinoic acid for invasive breast cancer.
Article Synopsis
- The major isoform of Flt1/VEGFR-1 in MDA-MB-231 breast cancer cells is a truncated intracellular isoform known as i21 Flt1, which enhances cell invasiveness by activating Src.
- The expression of i21 Flt1 is regulated by Notch signaling, as shown by its downregulation when treated with a γ-secretase inhibitor and siRNA targeting Notch-1 and Notch-3.
- Furthermore, the study indicates that retinoic acid can inhibit i21 Flt1 expression, suggesting a potential combined therapeutic strategy using γ-secretase inhibitors and retinoic acid to suppress this isoform in breast cancer.
Article Synopsis
- Two types of VEGFR-1 receptors exist: a full-length membrane receptor and a truncated soluble form (sVEGFR-1).
- Researchers have identified a new family of intracellular VEGFR-1 isoforms, specifically one called i(21)VEGFR-1, which is predominantly expressed in MDA-MB-231 breast cancer cells.
- The expression of i(21)VEGFR-1 increases the invasiveness of these cancer cells, and this process can be modulated by siRNA treatments and retinoic acid, which affects the activity of Src, a key signaling molecule.