Astatine-211 (²¹¹At) has emerged as a promising radionuclide for targeted alpha therapy of cancer by virtue of its favorable nuclear properties. However, the limited in vivo stability of ²¹¹At-labeled radiopharmaceuticals remains a major challenge. This review provides a comprehensive overview of the current strategies for ²¹¹At radiolabeling, including nucleophilic and electrophilic substitution reactions, as well as the recent advances in the development of novel bifunctional coupling agents and labeling approaches to enhance the stability of ²¹¹At-labeled compounds. The preclinical and clinical applications of ²¹¹At-labeled radiopharmaceuticals, including small molecules, peptides, and antibodies, are also discussed. Looking forward, the identification of new molecular targets, the optimization of ²¹¹At production and quality control methods, and the continued evaluation of ²¹¹At-labeled radiopharmaceuticals in preclinical and clinical settings will be the key to realizing the full potential of ²¹¹At-based targeted alpha therapy. With the growing interest and investment in this field, ²¹¹At-labeled radiopharmaceuticals are poised to play an increasingly important role in future cancer treatment.

Radioactive cesium (Cs) is a significant concern due to its role as a major byproduct of nuclear fission and its potential for radioactive contamination. Internal contamination with radioactive Cs is characterized by immoderate production of reactive oxygen species (ROS), resulting in severe radiation damage. Therefore, the development of therapeutic strategies should focus on enhancing the excretion of radioactive Cs and reducing radiation-induced oxidative damage. However, current therapeutic drugs like Prussian blue (PB) have limited efficacy in addressing these issues. In this study, we present Cu₃[Fe(CN)₆]₂ (CuFe) nanoparticles, a Prussian blue analog (PBA), which can not only efficiently sequester Cs but also exhibit resistance against radiation damage. The results of the adsorption studies demonstrate that CuFe outperforms PB in terms of adsorption performance. Further mechanistic investigations indicate that the increased adsorption capacity of CuFe may be attributed to the presence of additional defects resulting from the [Fe(CN)₆] missing linkers. Moreover, CuFe mimics the functions of catalase (CAT) and superoxide dismutase (SOD) by effectively eliminating O₂˙⁻ and H₂O₂ while scavenging ˙OH, thereby mitigating ROS induced by radiative Cs. Importantly, in vivo study confirms the efficient Cs decorporation capability of CuFe. The fecal cumulative excretion rate of CuFe reaches 69.5%, which is 1.45 times higher than that of PB (48.8%). These findings demonstrate that CuFe exhibits excellent Cs removal performance and ROS scavenging ability, making it an attractive candidate for the treatment of Cs contamination.

This paper presents a comprehensive review of recent advancements in radionuclide-labeled biomaterials for cancer therapy, with a particular focus on the characteristics, production methods, and labeling techniques of α-particle, β-particle, and Auger electron-based radiotherapy. It explores innovative strategies for targeted delivery systems and highlights the advantages of theranostics and combination therapies. The application of radionuclide-labeled biomaterials in various cancer types, including prostate cancer, breast cancer, neuroendocrine tumors, gliomas, and melanoma, is systematically summarized. Furthermore, the article critically examines current technological bottlenecks and challenges in clinical translation, while proposing future directions such as AI-assisted dose optimization and multimodal combination therapies. This review provides essential theoretical foundations and practical insights to facilitate the clinical translation of radionuclide-labeled biomaterials.

Uranium is a radioactive heavy metal and a significant public health concern; however, its associated underlying toxicological mechanisms remain largely unknown. In this work, the uptake and efflux processes of uranium in CHO-k1 cells were studied and the cytotoxicity effects were explored. It was found that both the uptake and efflux processes took place rapidly and half of the internalized uranium was expelled within 8 h. The uranium exposure caused a decrease of cell viability and adhesion ability in a dose-dependent manner and blocked the cell cycle at the G1 stage. In addition, gene expression analysis revealed relative changes in the transcription of metabolism related genes. Further studies revealed that the cytotoxicity of uranium could be alleviated by exposing cells to a lower temperature or by the addition of amantadine-HCl, an endocytosis inhibitor. Interestingly, after uranium exposure, needle-like precipitates were observed in both intracellular and extracellular regions. These findings collectively suggest that the cellular transport of uranium is a rapid process that disturbs cell metabolism and induces cytotoxicity, and this impact could be reduced by slowing down endocytic processes.

Long non-coding RNAs (lncRNAs) can be severed as competing endogenous RNAs (ceRNAs) to regulate target genes or mRNAs via sponging microRNAs (miRNAs). This study explored the effect of LINC01554 on liver cancer cells through the ceRNA mechanism. Five significantly down-regulated lncRNAs were selected for further verification, and then through bioinformatics, interactive miRNAs and mRNAs of lncRNAs were identified. The relationship between LINC01554, miR-148b-3p and EIF4E3 was detected by the dual luciferase reporter gene assay. Afterwards, HCCLM3 cells were transfected with pCDH-LINC01554, miR-148b-3p inhibitor and miR-148b-3p mimics. Cell viability, apoptosis, migration and invasion were measured by Cell Counting Kit-8, flow cytometer, and Transwell assays. Real-time quantitative PCR (RT-qPCR) and Western blot were used to measure the expressions of related genes and proteins. LINC01554 was significantly down-regulated in the liver cancer cell lines, and was expressed in the cytoplasm of HCCLM3 cells. LINC01554 overexpression inhibited proliferation, migration, and invasion of HCCLM3 cells, and promote their apoptosis (P < 0.05). Besides, LINC01554 overexpression also significantly increased the levels of BAX, BCL2/BAX, P53, cleaved-Caspase3, TIMP3, E-cadherin and EIF4E3 (P < 0.05). Through bioinformatics and dual-luciferase reporter gene assay, LINC01554, miR-148b-3p and EIF4E3 were proved to interact with each other. Furthermore, the effects of miR-148b-3p knockdown on HCCLM3 cells were similar with those of LINC01554 overexpression, and miR-148b-3p mimics could reverse the changes of cell viability, apoptosis, migration, and invasion induced by LINC01554 overexpression. LINC01554 overexpression could suppress the growth and metastasis of HCCLM3 cells via miR-148b-3p/EIF4E3.

Vascular endothelial cells produce reactive oxygen species (ROS) during the process of energy metabolism in aerobic respiration. A growing body of evidence indicates that excessive ROS is implicated in the pathogenesis of cardiovascular diseases including atherosclerosis. The newly synthesized halophenol, 2,4′,5′-trihydroxyl-5,2′-dibromo diphenylmethanone (TDD), exhibits antioxidative and cytoprotective activities in vitro. In this study, the protective effect of TDD against hydrogen peroxide (H₂O₂)-induced oxidative injury of EA.hy926 cells was investigated. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-dephenyltetrazolium bromide (MTT) assay, while the effect of TDD on the transcription profile of EA.hy926 cells subjected to H₂O₂-induced oxidative injury was evaluated by microarray analysis. Several signaling pathways, including apoptosis, were significantly associated with TDD. Flow cytometric analysis was used to evaluate anti-apoptotic effect of TDD. Subsequently, RT-PCR and Western blot were used to detect the expressions of the apoptosis-associated protein, Bcl-2 and Bax. Meanwhile the expression of cleaved caspase-3, an executioner of apoptosis, was also detected by Western blot. The results showed that pretreatment of EA.hy926 cells with TDD prevented the decrease of cell viability induced by H₂O₂, and attenuated H₂O₂-induced elevation of Bax and cleaved caspase-3 while increased Bcl-2 expressions. In summary, TDD inhibited H₂O₂-induced oxidative injury of EA.hy926 cells through negative regulation of apoptosis. These findings suggest that TDD is a potential candidate for therapeutic intervention in oxidative stress-associated cardiovascular diseases.