Samaneh Ahmadi

Cystic fibrosis (CF) is a severe inherited disorder caused by dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR), an epithelial ion channel essential for maintaining airway surface hydration and effective mucociliary clearance. Although over a thousand CFTR mutations have been described, their functional consequences vary widely, with some genotypes retaining partial CFTR activity and presenting as residual-function phenotypes. Despite CFTR modulator therapies substantially improved clinical outcomes in many patients, their efficacy remains incomplete and strongly dependent on the underlying CFTR mutation. Increasing evidence indicates that microRNAs (miRNAs), as key post-transcriptional regulators of gene expression, play a dual role in CF by contributing to disease pathogenesis while also representing potential therapeutic targets. This review provides an overview of the involvement of miRNAs in CF pathophysiology, with emphasis on their roles in CFTR regulation, airway inflammation, epithelial ion transport, and mucus homeostasis. Experimental findings demonstrating that modulation of specific miRNAs enhances CFTR mRNA stability and protein expression, attenuates pro-inflammatory signaling, and improves epithelial function are discussed. Current miRNA-based therapeutic strategies and their translational challenges are discussed, along with their potential integration with emerging CF therapies, including CFTR modulators, mRNA replacement, antisense oligonucleotides, and suppressor tRNA strategies. Given the predominantly preclinical evidence, miRNA modulation may offer a mutation-independent approach to complement existing therapeutic strategies. A combination of miRNA-based approaches with established CF therapies may represent a potential complementary strategy, but the efficacy and safety of such combinations require further experimental and clinical validation.

The cornea, as the essential part of the eye with the duty of maintaining transparency and vision, is susceptible to various diseases and genetic abnormalities. Vision loss due to corneal disorders is a global concern, prompting research into innovative treatment approaches. The investigations have provided a significant role that exosomes play in maintaining corneal homeostasis and promoting intercellular communication. The cornea is made up of cellular and acellular components. The cellular components include the epithelial cells, stromal keratocytes, and endothelial cells, which secrete exosomes that contribute to preserving corneal transparency, immune privilege, and tissue repair. These nanosized vesicles contain molecules that regulate immune responses, promote cell proliferation and migration, and protect against stress-induced cell death. In this review, we try to survey the therapeutic potential and effects of exosomes in treating various corneal conditions, which can contribute to enhance corneal healing, reduce scarring, and improve visual outcomes. Graphical Abstract

The glioblastoma multiform has some properties including rapid growth, invasion, treatment resistance, and recurrence. Therefore, new therapies need to be developed that can be approved for using in patients. The previous study showed Arsenic Trioxide inhibits aggressive behavior in glioblastoma cells. Also, (–)-epigallocatechin-3-gallate prevents cellular proliferation, and invasion in multiple glioma cells. Resveratrol decreases cellular proliferation, induces cell death, and impaired the invasiveness of glioma cells. Combination therapy to inhibit cancer cells may have important clinical implications. Therefore, to assess the combination therapy of 2μM Arsenic trioxide, 100μM EGCG, and 100μM Resveratrol, we examined the metabolic activity, colony formation, media pH, cell proliferation, Caspase 3 activity, and gene expression analysis of BCL2, Caspase 3, MMP2, MMP9, CA9, u-PA, u-PAR, and Cathepsin B genes in apoptosis and invasion by both quantitative PCR experiments and Western blot assay. Systems biology tools also were used to obtain, the related network, involved pathways, and identifying the key genes in our selected criteria. The results of the study confirmed that the combined therapy prevents cell proliferation and induces of apoptosis in the Brain tumor cell lines including: U87-MG, A-172, and 1321N1. Furthermore, over-expression of caspase-3 and down-regulation of BCL-2, MMP-2, and MMP-9 confirmed that combination therapy leads to induces apoptosis and decreases invasion. Nevertheless, the lowering of pharmacological doses and improving therapeutic efficacy through combination therapy may provide advantages to treat resistance cancer cells with lower side effects. Finally, the results might suggest new modality for Glioblastoma treatment.

Breast cancer, as the most frequent cancer diagnosed in women worldwide, is affected by different regulatory mechanisms and cellular processes such as micro ...