MicroRNA-203a inhibits breast cancer progression through the PI3K/Akt and Wnt pathways.

MicroRNA expression in breast cancer (BC) is explored both as a potential biomarker and for therapeutic purposes. Recent studies have revealed that miR-203a-3p is involved in BC, and importantly contributes to BC chemotherapy responses; however, the regulatory pathways of miR-203a in BC remain elusive. Hence, we aimed to investigate the miR-203a regulatory mechanisms and their potential functions in the progress of BC. To this end, the miR-203a potential involving pathways was predicted by databases analyzing its target genes. The relations between miR-203a, the phosphatidylinositol 3'-kinase (PI3K)-Akt, and Wnt signaling pathways were mechanistically investigated. Our results revealed that miR-203a inhibited the activation of the PI3K/Akt and Wnt pathways and reduced its downstream cell cycle signals, including Cyclin D1 and c-Myc. Moreover, the overexpression of miR-203a drastically arrested the cell cycle at subG1 and G1 phases, decreased the viability, proliferation, and migration, and increased apoptosis of BC cells. Therefore, miR-203a-3p may be considered a tumor suppressor factor and a potential biomarker or therapeutic target for BC.

Is there a relationship between homes' radon gas of MS and non-MS individuals, and the patients' paraclinical magnetic resonance imaging and visually evoked potentials in Yazd-Iran?

Long-term inhalation of radon gas can cause harm to humans and lead to many diseases. One of these diseases is multiple sclerosis (MS), the most common chronic disease of the central nervous system, which alters the brain structure and impedes the rapid transmission of nerve signals throughout the neuron system. Therefore, this study aimed to investigate the relationship of the radon gas concentration in residential homes of MS and non-MS individuals with their results of paraclinical MRI and VEP in Yazd City, Iran. The radon gas concentration was measured in residential homes of 44 people with MS and 100 healthy people. To this end, the questionnaire of radon gas monitoring in residential buildings was administered, and the radon gas concentration was measured by CR-39 detectors. The mean radon concentrations in the homes of MS and non-MS people were 69.51 and 70.83, respectively. A significant positive relationship was found between radon concentration and building's age (P = 0.038). Furthermore, radon concentration had a significant inverse relationship with the building's ventilation (P = 0.053) and cooling systems (P = 0.021). No significant relationship was observed between total radon concentration and MS incidence (P = 0.88). Moreover, no significant correlation was found between radon concentration and location of the plaque in MRI test results of the patients. However, it showed an inverse non-significant correlation with the plaque's number (r = - 0.12, P = 0.42). Further studies in this area are recommended.

Genome-Wide Studies of Rho5-Interacting Proteins That Are Involved in Oxidant-Induced Cell Death in Budding Yeast.

Rho GTPases play critical roles in cell proliferation and cell death in many species. As in animal cells, cells of the budding yeast Saccharomyces cerevisiae undergo regulated cell death under various physiological conditions and upon exposure to external stress. The Rho5 GTPase is necessary for oxidant-induced cell death, and cells expressing a constitutively active GTP-locked Rho5 are hypersensitive to oxidants. Yet how Rho5 regulates yeast cell death has been poorly understood. To identify genes that are involved in the Rho5-mediated cell death program, we performed two complementary genome-wide screens: one screen for oxidant-resistant deletion mutants and another screen for Rho5-associated proteins. Functional enrichment and interaction network analysis revealed enrichment for genes in pathways related to metabolism, transport, and plasma membrane organization. In particular, we find that ATG21, which is known to be involved in the CVT (Cytoplasm-to-Vacuole Targeting) pathway and mitophagy, is necessary for cell death induced by oxidants. Cells lacking Atg21 exhibit little cell death upon exposure to oxidants even when the GTP-locked Rho5 is expressed. Moreover, Atg21 interacts with Rho5 preferentially in its GTP-bound state, suggesting that Atg21 is a downstream target of Rho5 in oxidant-induced cell death. Given the high degree of conservation of Rho GTPases and autophagy from yeast to human, this study may provide insight into regulated cell death in eukaryotes in general.