Rong Rong

Hydrogel confinement stabilizes the Fe-MOF chromogenic microenvironment, enabling matrix-robust image-based screening of malathion in chemically heterogeneous Chinese medicinal extracts.

Multidrug resistance (MDR) is a major clinical challenge that limits the efficacy of multiple cancer treatment modalities, including chemotherapy, targeted therapy, immunotherapy, monoclonal antibody therapy, and antibody-drug conjugates. In recent years, exosomes (Exos), nanoscale vesicles involved in intercellular communication, have attracted increasing attention for their roles in the formation and spread of MDR. A growing body of evidence suggests that Exos mediate the transfer of resistance-related molecular signals among drug-resistant cancer cells, drug-sensitive cancer cells, and stromal cells, such as cancer-associated fibroblasts and tumor-associated macrophages, through the selective packaging of noncoding RNAs, functional proteins, and metabolic regulators. These molecular signals may induce the reprogramming of signaling pathways, metabolism, and epigenetic states in recipient cells, thereby promoting the acquisition of cancer stem cell-like properties and a drug-resistant phenotype. In turn, these changes may contribute to the establishment of a drug resistance-supporting tumor microenvironment. This review systematically summarizes the molecular mechanisms by which Exos contribute to multidrug resistance, with a particular focus on their roles in cargo sorting, microenvironmental crosstalk, and the functional reprogramming of recipient cells. It also discusses their potential for clinical translation in resistance monitoring and reversal therapy. In addition, this review further discusses the key challenges currently facing the field and provides perspectives on future research directions.

Influenza reporter viruses are essential for studying viral infection dynamics and assessing antiviral drug efficacy. However, insertion of exogenous reporter genes can impair both viral replication and reporter expression, limiting the development of these systems. In this study, CE1 compensatory mutation (G3A/C8U) was introduced into the 3′ non-coding region of the NS segment of influenza A/Puerto Rico/8/1934 using reverse genetics, generating the recombinant reporter virus H1N1-PR8-NS_CE1-mCherry. Compared with H1N1-PR8-NS_WT-mCherry, H1N1-PR8-NS_CE1-mCherry produced approximately 2.7-fold more infectious particles. CE1 compensatory mutation partially restored impaired replication kinetics in vitro, as evidenced by higher titers of H1N1-PR8-NS_CE1-mCherry at 48 h post-infection in MDCK cells. Additionally, H1N1-PR8-NS_CE1-mCherry maintained the intact mCherry gene insertion and high viral titers during serial passaging. Additionally, a real-time, non-invasive in vivo imaging of influenza A viruses was established using H1N1-PR8-NS_CE1-mCherry. A significant correlation was observed between lung fluorescence intensity and viral load, indicating that fluorescence signals serve as a reliable indicator of lung viral load in infected mice. Finally, utility of this model for in vivo drug screening was confirmed by antiviral drug oseltamivir phosphate. Above all, H1N1-PR8-NS_CE1-mCherry provides a tool for visualizing influenza A virus infection and evaluating antiviral drug efficacy.