Marco A. Velasco‐Velázquez

ORCID: 0000-0001-9717-0265
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Cancer Cells and Metastasis
  • Monoclonal and Polyclonal Antibodies Research
  • Cancer Mechanisms and Therapy
  • Autophagy in Disease and Therapy
  • Immunotherapy and Immune Responses
  • Computational Drug Discovery Methods
  • Metabolism, Diabetes, and Cancer
  • Cancer-related Molecular Pathways
  • Estrogen and related hormone effects
  • Radiopharmaceutical Chemistry and Applications
  • Epigenetics and DNA Methylation
  • Prostate Cancer Treatment and Research
  • Biosimilars and Bioanalytical Methods
  • Receptor Mechanisms and Signaling
  • Melanoma and MAPK Pathways
  • Cancer, Stress, Anesthesia, and Immune Response
  • Cell Adhesion Molecules Research
  • Crystallization and Solubility Studies
  • CAR-T cell therapy research
  • Protein purification and stability
  • X-ray Diffraction in Crystallography
  • Pancreatic function and diabetes
  • Chemokine receptors and signaling
  • Cancer, Lipids, and Metabolism
  • Immune Cell Function and Interaction

Universidad Nacional Autónoma de México
2016-2025

Brown Foundation
2023-2024

Institute for Social Security and Services for State Workers
2017-2022

Instituto Politécnico Nacional
2017-2020

Instituto Nacional de Psiquiatría
2020

Nobel Foundation
2020

Universidad Autónoma de la Ciudad de México
2020

Thomas Jefferson University
2011-2018

Tecnológico Nacional de México
2017

Consejo Nacional de Humanidades, Ciencias y Tecnologías
2017

The roles of the chemokine CCL5 and its receptor CCR5 in breast cancer progression remain unclear. Here, we conducted microarray analysis on 2,254 human specimens found increased expression CCR5, but not CCR3, basal HER-2 genetic subtypes. subpopulation cell lines to express displayed a functional response CCL5. In addition, oncogene transformation induced expression, cells that expressed also invasiveness. antagonists maraviroc or vicriviroc, developed block HIV coreceptor function, reduced...

10.1158/0008-5472.can-11-3917 article EN Cancer Research 2012-05-26

The rapid growth of COVID-19 cases is causing an increasing death toll and also paralyzing the world economy. De novo drug discovery takes years to move from idea and/or pre-clinic market, it not a short-term solution for current SARS-CoV-2 pandemic. Drug repurposing perhaps only solution, while vaccination middle-term solution. Here, we describe path HCV NS3-4A protease inhibitors boceprevir telaprevir as main (3CLpro) inhibitors. Based on our hypothesis that α-ketoamide drugs can...

10.1039/d0md00367k article EN cc-by-nc RSC Medicinal Chemistry 2020-12-21

Abstract Src family kinases (SFK) integrate signal transduction for multiple receptors, regulating cellular proliferation, invasion, and metastasis in human cancer. Although is rarely mutated prostate cancer, SFK activity increased the majority of cancers. To determine molecular mechanisms governing cancer bone metastasis, FVB murine epithelium was transduced with oncogenic v-Src. The cell lines metastasized mice to brain bone. Gene expression profiling tumors identified activation a CCR5...

10.1158/0008-5472.can-14-0612 article EN Cancer Research 2014-11-30

In recent years, immunomodulatory mechanisms of mesenchymal stem/stromal cells (MSCs) from bone marrow and other "classic" sources have been described. However, the phenotypic functional properties tumor MSCs are poorly understood. The aim this study was to analyze immunosuppressive capacity cervical cancer-derived (CeCa-MSCs) on effector T lymphocytes through purinergic pathway.We determined expression activity membrane-associated ectonucleotidases CD39 CD73 CeCa-MSCs normal tissue-derived...

10.1186/s12967-016-1057-8 article EN cc-by Journal of Translational Medicine 2016-10-26

Breast cancer stem cells (BCSCs) overexpress components of the Nuclear factor-kappa B (NF-κB) signaling cascade and consequently display high NF-κB activity levels. cell lines with proportion CSCs exhibit NF-κB-inducing kinase (NIK) expression. The role NIK in phenotype regulation is poorly understood. Expression was analyzed by quantitative RT-PCR BCSCs. levels were manipulated through transfection specific shRNAs or an expression vector. effect properties assessed mammosphere formation,...

10.1038/srep37340 article EN cc-by Scientific Reports 2016-11-23

Recently, we have shown that the CCL5/CCR5 axis is active in patients affected by an aggressive basal subtype of breast cancer. Using preclinical models, demonstrated CCR5 promotes cancer invasiveness and metastatic potential, while inhibition abrogates them. Thus, antagonists may constitute alternative therapeutic approach for

10.4161/onci.23660 article EN OncoImmunology 2013-04-01

Abstract Autophagy activated after DNA damage or other stresses mitigates cellular by removing damaged proteins, lipids, and organelles. Activation of the master metabolic kinase AMPK enhances autophagy. Here we report that cyclin D1 restrains autophagy modulating activation AMPK. In cell models human breast cancer in a D1–deficient model, observed D1–mediated reduction activation. Mechanistic investigations showed inhibited mitochondrial function, promoted glycolysis, reduced (pT172),...

10.1158/0008-5472.can-16-0425 article EN Cancer Research 2017-05-19

Changes in cytokine levels major depression and during treatment have been reported adults. However, few studies examined an adolescent sample despite this being a common age of onset. Methods . We measured proinflammatory (IL-2, IFN- γ , IL-1 β TNF- α IL-6, IL-12, IL-15) anti-inflammatory (IL-4, IL-5, IL-13, IL-1Ra, IL-10) serum 22 adolescents with 18 healthy volunteers. Cytokines were by multiplex bead-based immunoassays at baseline, 4 8 weeks after commencement fluoxetine administration...

10.1155/2018/4074051 article EN cc-by Mediators of Inflammation 2018-12-18

The SARS-CoV-2 viral spike protein S receptor-binding domain (S-RBD) binds ACE2 on host cells to initiate molecular events, resulting in intracellular release of the genome. Therefore, antagonists this interaction could allow a modality for therapeutic intervention. Peptides can inhibit S-RBD:ACE2 by interacting with protein-protein interface. In study, contact atlas data and dynamics simulations were used locate hotspots secondary structure elements α1, α2, α3, β3, β4 ACE2. We designed...

10.1021/acs.jmedchem.1c00477 article EN cc-by-nc-nd Journal of Medicinal Chemistry 2021-07-30

Introduction CD36 is a membrane receptor that participates in the cellular uptake of fatty acids and lipid metabolism. overexpression favors progression different pathologies, such as atherosclerosis cancer. Thus, targeting has medicinal relevance. Herein, we aimed to identify human anti-CD36 single-chain variable fragment (scFv) with therapeutic potential. Methods The semisynthetic ALTHEA Gold Plus Libraries™ were panned using recombinant CD36. Clone selection was performed by ELISA....

10.3389/fimmu.2025.1531171 article EN cc-by Frontiers in Immunology 2025-02-04

Background: Breast cancer (BrCa) patients with tumors expressing high interleukin-6 (IL6) levels have poor clinical outcomes. In BrCa, altered occupancy of CCCTC-binding factor (CTCF) within its DNA binding sites deregulates the expression targeted genes. this study, we investigated whether CTCF contributes to IL6 in BrCa. Methods/Results: We performed gain- and loss-of-function assays BrCa cell lines observed an inverse correlation between levels. To understand how negatively regulates gene...

10.3390/ph18030305 article EN cc-by Pharmaceuticals 2025-02-23
Coming Soon ...