Browse Articles
Discover research articles across all indexed journals
Enantioselective Synthesis of Spirocyclic Nitrogen-Containing Heterocycles Catalyzed by an Iridium-Containing Cytochrome
Identifying key factors for organizational resilience among medical alliance using the analytic hierarchy process method
Bumps on the Road: The Way to Clean Relaxation Dispersion Magic-Angle Spinning NMR
Comprehensive evaluation of impact strength and microstructural characteristics of geopolymer concrete reinforced with four types of natural fibers of varying lengths
Regulating the Acidity of HF/Pyridine Media to Control the Chemodivergent Fluoro- and Hydro-Heteroalkylation of Olefins
Publisher Correction: Effects of intranasal neural stem cells transplantation on olfactory epithelium regeneration in an anosmia-induced mouse model
Electrochemical Oxygen Reduction Reaction-Coupled Dechlorination Promoting Acylation Reaction for Aromatic Ester Synthesis
π–π Stacking and Structural Configurations in Aromatic Thiophene and Fluorobenzene Dimers Revealed by Rotational Spectroscopy
LINC00162 silencing enhances sorafenib sensitivity and inhibits thyroid cancer cells progression through modulation of MAPK signaling and apoptosis
Abstract Many studies have reported the aberrant expression of lncRNAs and indicated their role in cancer progression and drug resistance across various cancers. In this study, we aimed to evaluate the effect of LINC00162 lncRNA on the chemosensitivity of thyroid cancer cells, both individually and in combination with sorafenib, on various biological processes. In this regard, we conducted our experiments in several groups: (1) LINC00162 siRNA-transfected cells, (2) Sorafenib-treated cells, (3) Cells that received both siRNA transfection and sorafenib treatment (4) Control group. MTT assay results revealed that siRNA-mediated silencing of LINC00162 reduced the viability of the B-CPAP thyroid cancer cells and increased the sensitivity of these cells to sorafenib by reducing its IC50. Flow cytometry analysis of apoptosis and cell cycle progression indicated that LINC00162 silencing induced apoptosis and Sub-G1 cell cycle arrest, while its combination with sorafenib significantly increased the apoptosis rate and also arrested cells in the G2-M phase in addition to the Sub-G1 phase. This combination treatment increased the expression of apoptosis-related genes BAX, CASP3, CASP9 while decreasing BCL2 expression. Additionally, significant inhibition of the cell-cycle related genes MYC and Cyclin D and upregulation of TP53 were observed following combination treatment. Furthermore, the combination therapy reduced the migration of B-CPAP cells through the downregulation of MMP-3 and MMP-9. Colony sizes and numbers also decreased following siRNA-mediated silencing of LINC00162 and sorafenib treatment. qRT-PCR analysis of stemness-related genes, including NANOG, SOX2, CD44, and CD133 confirmed the findings of the colony formation assay. To understand the underlying mechanisms of LINC00162 lncRNA in thyroid cancer progression, we evaluated the expression of MAPK pathway genes. Our findings indicated that LINC00162 silencing, in combination with sorafenib, reduced the expression of MAPK, KRAS, and RAF genes. From our findings, we can conclude that LINC00162 silencing, both individually and combined with sorafenib, reduced the progression and viability of thyroid cancer cells through modulating genes involved in key pathways and could be considered a new therapeutic approach for the treatment of papillary thyroid cancer (PTC).
Unveiling the Angstrom-Scale Interfacial Electron Spillover through the Metal/Electrolyte Interface
Tailored manganese oxide and nickel sulfide composites with MWCNTs as platinum-free electrodes for solar energy conversion
Tunable Formal Photocycloaddition of 1-Naphthol Derivatives
Benevolent leadership enhances organizational learning through communication, trust, and knowledge sharing
Abstract This research addresses a significant gap in existing literature, which predominantly focuses on mainstream leadership styles, like transactional or transformational leadership. It illustrates how benevolent leadership, characterized by warmth and a paternalistic approach, can foster environments conducive to knowledge sharing and organizational learning. Utilizing a survey of 350 respondents from various knowledge-intensive organizations, the study employs structural equation modelling to analyze the data. The findings challenge the conventional belief that benevolent leadership inherently promotes a learning environment, suggesting that its effectiveness is significantly amplified when combined with trust and open communication. This study contributes to theoretical advancements by integrating social exchange theory with organizational learning, highlighting that the reciprocity triggered by benevolent leadership encourages employees to engage in positive knowledge-sharing behaviors, thereby enhancing organizational learning capabilities. For practitioners, these insights emphasize the importance of nurturing leadership styles that support trust and openness to foster a culture where knowledge is freely shared, thus enhancing the organization’s ability to adapt and innovate.
Nanographene-Oxy Radical Stabilized by a Carbaporphyrin Framework
Chondroitin sulfate protects against synaptic impairment caused by fluorosis through the Erk1/2-MMP-9 signaling pathway
Abstract Prolonged exposure to fluoride may induce neurotoxic effects. Chondroitin sulfate (CS) exhibits protective functions within the central nervous system (CNS); however, the mechanism by which CS protects synapses against fluoride remains incompletely understood. Our objective was to investigate the protective efficacy of CS on synapses and decipher its underlying mechanisms. We showed that fluoride exposure reduced the expression of synaptic protein synaptophysin (SYN) and impaired learning and memory functions, whereas CS counteracted these alterations, suggesting its protective effect against fluoride-induced cognitive deficits. Further studies revealed disruption of the Erk1/2/MMP-2/MMP-9 signaling pathway both in vivo and in vitro, manifested by increased total Erk1/2, Erk1/2 phosphorylation and MMP-9 expression, along with decreased MMP-2 levels. Importantly, treatment of SH-SY5Y cells with PD98059 or CS attenuated fluoride-induced effects, indicating a regulatory role of CS in the Erk1/2/MMP-9 signaling pathway. However, MMP-2 was not implicated in this process. These data demonstrate the neuroprotective effects of CS and highlight its potential for protecting against fluoride-induced neurotoxicity and synaptic impairment.