Quiescent cancer cells (QCCs) are considered an origin of cancer recurrence and present an ongoing challenge in cancer treatment. Following anti-cancer therapy, non-proliferating, therapy-resistant QCCs have been detected as subsets of residual cancer cells within patients. Clinicians and researchers widely believe that these minimal residual QCCs can eventually regain proliferative activity, acting as "seeds" for cancer recurrence. Despite the significance of QCCs, tracing and analyzing these microscopic residual cells in vivo models and patients remains extremely challenging, limiting our understanding. Consequently, reliable biomarkers for QCCs and the mechanisms underlying their 'reversible' reactivation are still poorly understood. This knowledge gap has hindered the development of diagnostics and targeted therapies for QCCs. The absence of diagnostic tools for QCCs also complicates predicting cancer relapse and determining the optimal duration of anti-cancer treatment. Moreover, without strategies to eradicate QCCs, preventing cancer recurrence remains elusive. This review aims to provide an overview of the current understanding of QCCs and related diagnostic efforts in both basic and clinical research. Additionally, potential strategies for the targeted elimination of QCCs are explored. Focused research and clinical attention to diagnosing and eradicating residual QCCs are essential for preventing cancer recurrence and ultimately conquering this deadly disease.

Base editors, including adenine base editors (ABEs) and cytosine base editors (CBEs), are widely used in numerous organisms to introduce site-specific sequence modifications in genomic DNA without causing double-strand breaks (DSBs). However, these editors exhibit low editing efficiencies, particularly in dicot plants, thereby limiting their application in dicot plant genome engineering. In this study, we assessed the editing efficiencies of various base editors to identify those optimal for base editing in dicot plants. We discovered that ABE8e, an ABE variant, demonstrated superior A-to-G base editing efficiency within A5-A8 windows, and A3A/Y130F-V04, a CBE variant, exhibited the highest C-to-T base editing efficiency within C4-C15 windows in both Arabidopsis and soybean protoplasts. Overall, we recommend these two base editors as prime choices for efficient genome engineering in a range of crop plants.

Accumulating data have shown that targeting breast cancer stem cells (CSCs) is an auspicious way for anticancer therapies. This study demonstrated that the antirheumatic drug auranofin is a potent CSC inhibitor with anti-CSC action on breast cancer. This research focused on investigating the effect of auranofin on breast cancer and CSCs and its cellular mechanism. Mammosphere formation, colony formation, levels of CD44^high/CD24^low, and aldehyde dehydrogenase 1 expression in the cells were evaluated after auranofin treatment. The anti-CSC properties of auranofin were further examined by gel shift assay and cytokine detection. Auranofin suppressed cell growth, colony formation, migration, and mammosphere formation and triggered apoptosis in breast cancer. Auranofin decreased the CD44^high/CD24^low- and aldehyde dehydrogenase-expressed subpopulations, as well as the Stat3-DNA interaction and phosphorylated Stat3 level. Auranofin also decreased the extracellular levels of interleukin-8 (IL-8) in the mammosphere media. Auranofin suppressed the Stat3/IL-8 signal and killed CSCs; therefore, it may be a potential target for CSCs.

Diesel exhaust particles (DEPs), a major component of air pollution, are well-known to induce inflammation and vascular dysfunction. However, the molecular mechanisms linking DEP exposure to the disruption of the blood-retina barrier (BRB) remain poorly understood. Toll-like receptors (TLRs), particularly TLR2 and TLR4, play critical roles in inflammatory signaling and may contribute to DEP-induced retinal endothelial dysfunction. This study investigates the involvement of TLR2 and TLR4 in mediating DEP-induced disruption of the BRB and evaluates the protective effects of TLR inhibition using both in vitro and in vivo experiments. U937 human macrophages were exposed to DEPs of ultrafine size (＜0.2 ㎛), and the mRNA expression of TNF-α and IL-1β was quantified. Conditioned media from DEP-exposed U937 cultures were then used to treat human retinal endothelial cells (HRECs). DEP exposure significantly increased TNF-α and IL-1β mRNA expression in U937 macrophages. Conditioned media from DEP-exposed U937 macrophages reduced claudin-5 and ZO-1 expression in HRECs, resulting in increased BRB permeability. Inhibition of TLR2 and TLR4 using C29 and TAK242, respectively, significantly attenuated TNF-α and IL-1β mRNA expression in DEP-exposed U937 macrophages and preserved BRB integrity by maintaining claudin-5 and ZO-1 expression in HRECs. In the mouse model, DEP exposure caused a marked reduction in claudin-5 and ZO-1 levels in retinal vessels, whereas treatment with C29 and TAK242 mitigated the loss of these tight junction proteins. This study demonstrates that DEPs induce inflammation and BRB dysfunction through TLR2 and TLR4 activation, leading to increased vascular permeability and potential retinal damage. Furthermore, TLR2 and TLR4 inhibition may be a promising therapeutic strategy to protect retinal health from air pollution-induced damage.

Glioblastoma (GBM) frequently expresses cytomegalovirus (CMV) antigens, making CMV-specific CD8⁺T cells attractive candidates for adoptive immunotherapy due to their longevity and inherent tumor reactivity. However, these T cells encounter significant immunosuppressive challenges within the GBM microenvironment, including cytokine scarcity and checkpoint-mediated inhibition, which limit their proliferation and function. Here, we assessed strategies to overcome these limitations by modulating immune checkpoint pathways. Antigen stimulation combined with IL-2 robustly expanded high-avidity (tetramer-high) CMV-specific T cells with significant enrichment of CD62L⁺ central memory (TCM) cells. In contrast, antigen stimulation alone modestly expanded tetramer-high cells with limited TCM enrichment. PD-L1 blockade in the absence of IL-2 favored expansion of tetramer-high CMV-specific CD8⁺T cells, preserved CD62L expression, and enhanced CD226 expression. Furthermore, combining anti-PD-L1 blockade with an anti-CD226 agonist markedly enhanced proliferation, IFN-γ production, and TCM enrichment in both tetramer-high and tetramer-low populations, reaching levels comparable to IL-2-supported conditions. Together, these findings highlight that simultaneous modulation of PD-L1 and CD226 pathways can restore CMV-specific T cell function, offering a promising strategy to boost TCR-T efficacy in cytokine-deprived environments.