RESUMEN
The capture of radioactive iodine species from nuclear waste is crucial for environmental protection and human health. Porous organic cages (POCs), an emerging porous material, have showed potential in iodine adsorption due to the advantages of tunable pores and processibility. However, integrating multiple desirable characteristics into a single POC through bottom-up assembly of pre-designed building blocks remains challenging. Post-synthetic modification (PSM) offers an alternative approach, enabling the introduction of various functions into a single POC. Herein, a viable and highly efficient three-step PSM strategy to modify a representative POC (CC3), is presented. The modified POC, OFT-RCC36+6Br-, features a charged confined space, electron-rich heteroatom, and halide ions, exhibiting significantly enhanced iodine vapor uptake compared to the parental cage. The universality of the PSM strategy has been verified by successfully modifying two other POCs. The iodine adsorption behaviors of three modified cage adsorbents in organic solvent and aqueous solution have also been investigated, all of which exhibited improved performance, especially in comparison to ionic cages modified through direct protonation. This work provides an effective PSM strategy for POCs to facilitate iodine adsorption. More importantly, the introduction of a new PSM strategy enriches the functional diversity of POCs, potentially broadening their future applications.
RESUMEN
Cancer metastatic organotropism is still a mystery. The liver is known to be susceptible to cancer metastasis and alcoholic injury. However, it is unclear whether and how alcohol facilitates liver metastasis and how to intervene. Here, we show that alcohol preferentially promotes liver metastasis in colon-cancer-bearing mice and post-surgery pancreatic cancer patients. The mechanism is that alcohol triggers an extra- and intrahepatic crosstalk to reshape an immunosuppressive liver microenvironment. In detail, alcohol upregulates extrahepatic IL-6 and hepatocellular IL-6 receptor expression, resulting in hepatocyte STAT3 signaling activation and downstream lipocalin-2 (Lcn2) upregulation. Furthermore, LCN2 promotes T cell-exhaustion neutrophil recruitment and cancer cell epithelial plasticity. In contrast, knocking out hepatocellular Stat3 or systemic Il6 in alcohol-treated mice preserves the liver microenvironment and suppresses liver metastasis. This mechanism is reflected in hepatocellular carcinoma patients, in that alcohol-associated signaling elevation in noncancerous liver tissue indicates adverse prognosis. Accordingly, we discover a novel application for BBI608, a small molecular STAT3 inhibitor that can prevent liver metastasis. BBI608 pretreatment protects the liver and suppresses alcohol-triggered premetastatic niche formation. In conclusion, under extra- and intrahepatic crosstalk, the alcoholic injured liver forms a favorable niche for cancer cell metastasis, while BBI608 is a promising anti-metastatic agent targeting such microenvironments.