Obtention of biochar-Ca nanoparticles using Citrus tangerina׃ A morphological, surface and study remotion of Aflatoxin AFB1.

This work presents the formation of biochar with calcium nanoparticles (NPsCa) in function of pyrolysis time (C10, C30, C60, C120 and C180 min) using the Citrus tangerina peel and their evaluation in the remotion of Aflatoxin B1 (AFB1) in aqueous phase. Firstly, the Citrus tangerina was studied by Thermogravimetric analysis to determine the optimal temperature (TGA), obtaining a result of 600 °C. The biochar (NPsCa) were characterized by Scanning Electronic Microscopy (SEM) and Energy Dispersive Spectroscopy (EDS), as well as surface properties including the identification of functional groups by Fourier Transform Infrared Spectrometry (FTIR), and energetic states through the X-Ray Photoelectron Spectroscopy (XPS). The adsorption studies were carried out on the different materials and later, the experimental data was adjusted to different mathematical models, obtaining the best fit of the kinetic data to the Ho-McKay model, whilst the adsorption isotherms were adjusted to the model of Langmuir, which indicates that the Aflatoxin B1 adsorption process is carried out through a monolayer chemisorption process with maximum sorption capacities (qm) ranging between 15.72 and 63.22 µg g-1 with the 180th minute being the adequate time to obtain the carbon with the best surface properties and the best adsorption capacity. Additionally, it was observed that each material can be reused up to five times in accordance with the results from the reuse cycles.

Obtention of biochar-Fe/Ce using Punica granatum with high adsorption of ampicillin capacity.

This research presents the obtaining of a biochar (CB) from the use of pomegranate peel (Punica granatum) conditioned with iron and cerium nanoparticles (C-Fe/Ce), as well as its characterization by SEM (Scanning Electronic Microscopy), FTIR (Fourier Transform Infrared Spectrometry), TGA (Thermogravimetric analysis), EDS (Energy Dispersive Spectroscopy), XPS (X-Ray Photoelectron Spectroscopy) and evaluation of the adsorption capacity of ampicillin (AMP) in aqueous phase at 20, 30 and 40 °C. The maximum adsorption capacity for CB was 18.97 mg g-1 and for C-Fe/Ce, 27.61 mg g-1 at pH of 7, observing that with increasing temperature, the sorption capacity decreases in both materials, the experimental data was fitted to various mathematical models and the best fit was the pseudo-second order model for the kinetics, whilst for the adsorption isotherms the best fit was with the Langmuir model, indicating that the adsorption process is carried out in a monolayer on a homogeneous surface, through a chemisorption process. According to the thermodynamic parameters this process is carried out through an exothermic reaction. The results obtained indicate that both materials are suitable for the removal of AMP in the aqueous phase and that they can be reused up to 5 times.

An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer.

Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future.

Loss of Tribbles pseudokinase-3 promotes Akt-driven tumorigenesis via FOXO inactivation.

Tribbles pseudokinase-3 (TRIB3) has been proposed to act as an inhibitor of AKT although the precise molecular basis of this activity and whether the loss of TRIB3 contributes to cancer initiation and progression remain to be clarified. In this study, by using a wide array of in vitro and in vivo approaches, including a Trib3 knockout mouse, we demonstrate that TRIB3 has a tumor-suppressing role. We also find that the mechanism by which TRIB3 loss enhances tumorigenesis relies on the dysregulation of the phosphorylation of AKT by the mTORC2 complex, which leads to an enhanced phosphorylation of AKT on Ser473 and the subsequent hyperphosphorylation and inactivation of the transcription factor FOXO3. These observations support the notion that loss of TRIB3 is associated with a more aggressive phenotype in various types of tumors by enhancing the activity of the mTORC2/AKT/FOXO axis.

The orphan receptor GPR55 drives skin carcinogenesis and is upregulated in human squamous cell carcinomas.

G protein-coupled receptors (GPCRs) control crucial physiological processes and their dysfunction contributes to various human diseases, including cancer. The orphan GPCR GPR55 was identified and cloned more than a decade ago, but very little is known about its physio-pathological relevance. It has been recently shown that GPR55 controls the behavior of human cancer cell lines in culture and xenografts. However, the assessment of the actual role of this receptor in malignant transformation in vivo is hampered by the lack of studies on its functional impact in clinically-relevant models of cancer. Here we demonstrate that GPR55 drives mouse skin tumor development. Thus, GPR55-deficient mice were more resistant to DMBA/TPA-induced papilloma and carcinoma formation than their wild-type littermates. GPR55 exerted this pro-tumor effect primarily by conferring a proliferative advantage on cancer cells. In addition, GPR55 enhanced skin cancer cell anchorage-independent growth, invasiveness and tumorigenicity in vivo, suggesting that it promotes not only tumor development but also tumor aggressiveness. Finally, we observed that GPR55 is upregulated in human skin tumors and other human squamous cell carcinomas compared with the corresponding healthy tissues. Altogether, these findings reveal the pivotal importance of GPR55 in skin tumor development, and suggest that this receptor may be used as a new biomarker and therapeutic target in squamous cell carcinomas.

The orphan G protein-coupled receptor GPR55 promotes cancer cell proliferation via ERK.

GPR55 is an orphan G protein-coupled receptor that may be engaged by some lipid ligands such as lysophosphatidylinositol and cannabinoid-type compounds. Very little is known about its expression pattern and physio-pathological relevance, and its pharmacology and signaling are still rather controversial. Here we analyzed the expression and function of GPR55 in cancer cells. Our data show that GPR55 expression in human tumors from different origins correlates with their aggressiveness. Moreover, GPR55 promotes cancer cell proliferation, both in cell cultures and in xenografted mice, through the overactivation of the extracellular signal-regulated kinase cascade. These findings reveal the importance of GPR55 in human cancer, and suggest that it could constitute a new biomarker and therapeutic target in oncology.