A5053683692- Glioma Diagnosis and Treatment
- Adenosine and Purinergic Signaling
- PI3K/AKT/mTOR signaling in cancer
- Protein Kinase Regulation and GTPase Signaling
- Mechanisms of cancer metastasis
- Epigenetics and DNA Methylation
- Drug Transport and Resistance Mechanisms
- Nanoplatforms for cancer theranostics
- Wnt/β-catenin signaling in development and cancer
- MicroRNA in disease regulation
- Pancreatic and Hepatic Oncology Research
- 14-3-3 protein interactions
- Brain Metastases and Treatment
- Cancer-related gene regulation
- Inflammatory mediators and NSAID effects
- Nitric Oxide and Endothelin Effects
- Caveolin-1 and cellular processes
- Cancer Mechanisms and Therapy
- Histone Deacetylase Inhibitors Research
- Protease and Inhibitor Mechanisms
- Virus-based gene therapy research
- Autophagy in Disease and Therapy
- Cancer therapeutics and mechanisms
- Cancer Cells and Metastasis
- Extracellular vesicles in disease
Austral University of Chile
2017-2024
University of Chile
2010-2023
Millennium Institute on Immunology and Immunotherapy
2022-2023
Abstract Protein kinase CK2 is a highly conserved and constitutively active Ser/Thr-kinase that phosphorylates large number of substrates, resulting in increased cell proliferation survival. A known target Akt, player the PI3K/Akt/mTORC1 signaling pathway, which aberrantly activated 32% colorectal cancer (CRC) patients. On other hand, mTORC1 plays an important role regulation protein synthesis, growth, autophagy. Some studies suggest regulates several cancers. The most recently developed...
β-Catenin is a key protein in the canonical Wnt signaling pathway and many cancers alterations transcriptional activity of its components are observed. This up-regulated by kinase CK2, but underlying mechanism this change unknown. It has been demonstrated that CK2 hyperactivates AKT/PKB phosphorylation at Ser129, AKT phosphorylates β-catenin Ser552, which turn, promotes nuclear localization activity. However, consequences CK2-dependent hyperactivation on cell viability have not evaluated. We...
Glioblastoma (GBM) is a neoplasm characterized by an extensive blood vessel network. Hypoxic niches of GBM can induce tumorigenic properties small cell subpopulation called stem-like cells (GSCs) and also increase extracellular adenosine generation which activates the A₃ receptor (A₃AR). Moreover, GSCs potentiates persistent neovascularization in GBM. The aim this study was to determine if A₃AR blockade reduce vasculogenesis mediated differentiation Endothelial Cells (ECs) under hypoxia. We...
Abstract Augmented expression of protein kinase CK2 is associated with hyperproliferation and resistance to apoptosis in cancer cells. Effects are at least partially linked signaling via the Wnt/β‐catenin pathway, which dramatically enhanced colon cancer. Cyclooxygenase‐2 (COX‐2), a target gene, has been progression metastasis. However, possibility that connection may exist between COX‐2 not explored previously. Here we investigated changes activity upon modulation evaluated how these...
// Ignacio Niechi 1 , Eduardo Silva Pablo Cabello Hernan Huerta Valentina Carrasco Paulina Villar Luis Rodrigo Cataldo Katherine Marcelain 2 Ricardo Armisen Manuel Varas-Godoy 3 Cristina Fernandez 4 Julio C. Tapia 1, Cell Transformation Laboratory, Program of Cellular and Molecular Biology, ICBM, Faculty Medicine, University Chile, Santiago, Chile Fundacion Ciencia y Vida, Department Anatomopathology, HCUCH, Correspondence to: Tapia, e-mail: jtapia@med.uchile.cl Keywords: CK2, ECE-1,...
Glioblastoma (GBM) is the most common and aggressive type of brain tumor due to its elevated recurrence following treatments. This mainly mediated by a subpopulation cells with stemness traits termed glioblastoma stem-like (GSCs), which are extremely resistant anti-neoplastic drugs. Thus, an advancement in understanding molecular processes underlying GSC occurrence should contribute significantly towards progress reducing aggressiveness. High levels endothelin-converting enzyme-1 (ECE1), key...
The endothelin-1 (ET-1) axis contributes to the pathophysiology of several cancers by promoting tumor development and progression. This peptide is activated from its precursor, big ET-1, endothelin-converting enzyme-1 (ECE-1). Active ET-1 binds cognate G-coupled receptor, ETAR, which transduces signal inside cell. has a short half-life about 90 s, so biological effects are completely dependent on enzymatic activation ECE-1. Expression ECE-1 elevated in tumors cancer cell lines. There four...
Glioblastoma is the brain tumor with worst prognosis. This mainly due to a cell subpopulation an extremely aggressive potential, called glioblastoma stem-like cells (GSCs). These produce high levels of extracellular adenosine, which are increased even more under hypoxic conditions. Under hypoxia, adenosine signaling related HIF-2α expression, enhancing aggressiveness. Adenosine can be degraded using recombinant deaminase (ADA) revert its pathological effects. The aim this study was degrade...
Poor response to current treatments for glioblastoma has been attributed the presence of stem-like cells (GSCs). GSCs are able expel antitumor drugs extracellular medium using multidrug resistance-associated protein 1 (MRP1) transporter. Tacrolimus (FK506) identified as an MRP1 regulator in differentiated (GBM) (non-GSCs); however, effect FK506 on is currently unknown. The objective following research evaluate MRP1-related chemo-resistant phenotype GSCs. For this, U87MG and C6 glioma cell...
Endothelin‐1 is a mitogenic peptide that activates several proliferation, survival, and invasiveness pathways. The effects of endothelin‐1 rely on its activation by endothelin‐converting enzyme‐1 (ECE1), which expressed as four isoforms with different cytoplasmic N termini. Recently, isoform ECE1c has been suggested to have role in cancer aggressiveness. terminus phosphorylated protein kinase CK2 (also known casein 2), this enhances stability promotes colorectal cells. However, it not how...
Glioblastoma (GBM) is the most common and deadly malignant brain tumor, with a median survival of 15 to 17 months for patient. GBM contains cellular subpopulation known as stem-like cells (GSCs) that persist in hypoxic niches are capable infiltrating into healthy tissue. For this reason, GSCs considered one main culprits recurrence. A microenvironment increases extracellular adenosine levels, activating low affinity A2B receptor (A2BAR). Adenosine, through A2BAR, modulating invasiveness....
Gallbladder cancer (GBC) is a rare pathology in Western countries. However, it constitutes relevant health problem Asia and Latin America, with high mortality middle-aged Chilean women. The limited therapeutic options for GBC require the identification of targetable proteins prognostic value improving clinical management support. We evaluated expression proteins, including three epithelial tumor markers, four associated multidrug apoptosis resistance, eleven immunological markers 241 primary...
Endothelin-converting enzyme-1 (ECE1) activates the endothelin-1 peptide, which upregulates pathways that are related to diverse hallmarks of cancer. ECE1 is expressed as four isoforms differing in their N-terminal domains. Protein kinase CK2 phosphorylates N-terminus isoform ECE1c, enhancing its stability and promoting invasiveness colorectal cancer cells. However, specific residues ECE1c phosphorylated by how this phosphorylation promotes was unknown. Here we demonstrate Ser-18 Ser-20 bona...
Glioblastoma is the most common and aggressive primary brain tumor, characterized by its high chemoresistance presence of a cell subpopulation that persists under hypoxic niches, called glioblastoma stem-like cells (GSCs). The GSCs mediated in part adenosine signaling ABC transporters, which extrude drugs outside cell, such as multidrug resistance-associated proteins (MRPs) subfamily. Adenosine promotes MRP1-dependent normoxia. However, adenosine/MRPs-dependent hypoxia has not been studied...
Abstract Background Lung cancer constitutes the leading cause of mortality. High levels endothelin-1 (ET-1), its cognate receptor ET A R and activating enzyme, endothelin-converting enzyme-1 (ECE-1), have been reported in several types, including lung cancer. ECE-1 comprises four isoforms, which only differ their cytoplasmic N-terminus. Protein kinase CK2 phosphorylates N-terminus isoform ECE-1c, increasing stability to enhanced invasiveness glioblastoma colorectal cells, is believed be...