Signaling crosstalk of Galectin-3, β-catenin, and estrogen receptor in androgen-independent prostate cancer DU-145 cells.

The aims of this study were to investigate the localization of non-phosphorylated β‑catenin and Galectin-3 (GAL-3), the regulation of the expression of both proteins by activation of estrogen receptors (ERs) and their role in tumorigenic characteristics of androgen-independent prostate cancer DU-145 cells. DU-145 cells were cultured in the absence (control), and presence of 17β-estradiol (E2). Cells were also untreated or pre-treated with the inhibitor of GAL‑3, VA03, or with a compound that disrupts the complex β-catenin-TCF/LEF transcription factor, PKF 118-310.

Microglia in the aged brain develop a hypoactive molecular phenotype after surgery.

Background: Microglia, the resident immune cells of the brain, play a crucial role in maintaining homeostasis in the central nervous system (CNS). However, they can also contribute to neurodegeneration through their pro-inflammatory properties and phagocytic functions. Acute post-operative cognitive deficits have been associated with inflammation, and microglia have been implicated primarily based on morphological changes.

Valorization of agro-industrial wastes of sugarcane bagasse and rice husk for biosorption of Yellow Tartrazine dye.

The use of agro-industrial wastes as biosorbents is a promising alternative for sustainable, economical and effective adsorption. However, few studies evaluate the use of Brazilian agro-industrial waste as biosorbents without physicochemical pre-treatment. This study explored the potential of sugarcane bagasse (SCB) and rice husk waste (RHW) as low-cost biosorbents for yellow tartrazine dye removal.

Estrogen receptor activates SRC and ERK1/2 and promotes tumorigenesis in human testicular embryonic carcinoma cells NT2/D1.

Testicular germ cell tumors have the highest incidence in young men (between 15 and 44 years of age) and its etiology is still unclear, but its emergence on puberty suggests a hormone-dependent mechanism for the development of these tumors and their progression. We previously identified the estrogen receptor ESR1, ESR2, GPER and an isoform of ESR1, the ESR1-36 in human testicular embryonic carcinoma NT2/D1 cells, and the activation of SRC induced by ESR1 and ESR2 in these cells. Therefore, this study aimed to analyze the role of ER in the activation of ERK1/2, and the involvement of SRC and ERK1/2 on proliferation, migration, and invasion of the NT2/D1 cells.