Organic afterglow materials based on carbon dots (CDs) have aroused extensive attention for their potential applications in sensing, photoelectric devices, and anticounterfeiting. Effective methods to control the CD structure and modulate the energy levels are critical but still challenging. Here, we demonstrate a method to modulate the afterglow emission of CDs@SiO2 composites by controlling the carbonization degree of CDs with variable calcining temperatures. The CDs@SiO2-Raw prepared with a hydrothermal bottom-up synthesis method shows a more polymerized structure of CDs with low carbonization degree, which emits long-lived thermally activated delayed fluorescence (TADF) with the lifetime of 252 ms. After calcination at 550 °C, CDs@SiO2-550 exhibits a larger conjugated π-domain structure with higher carbonization degree, thus inducing room-temperature phosphorescence (RTP) emission with a lifetime of 451 ms. The transformation of the carbonization degree of CD structures leads to changes in energy levels and ΔE ST, which affect their afterglow luminescence behaviors. This work proposes a new concept to modulate the afterglow emission of CDs@SiO2 composites and forecasts potential applications of CD-based afterglow materials.
Background: Accumulating evidence indicates the essential role of EPHX2 in tumorigenesis. However, to date, no studies have performed a systematic evaluation of EPHX2 gene in human cancers and the predictive role of EPHX2 in cancer immunotherapy response has still not been explored. Methods: In the present study, Oncomine, TIMER2, UALCAN, GEPIA2, PrognoScan, HPA and Kaplan-Meier Plotter database were utilized to comprehensively analyze the expression landscape and prognostic clinical value of EPHX2 across 33 human cancers. To gain a better understanding of the role of EPHX2 in cancer immunotherapy, the correlations between EPHX2 and tumor immune microenvironment (TME) such as immune cell infiltrations, immune modulators, and the major histocompatibility complex were demonstrated. The underlying EPHX2-associated signaling pathways in cancer were also analysed. Moreover, the correlation between EPHX2 and immunotherapeutic biomarkers such as tumor mutational burden (TMB) and microsatellite instability (MSI) was explored. At last, the potential immune checkpoint blockers (ICB) response was predicted using tumor immune dysfunction and exclusion (TIDE) algorithm. Results: Overall, the mRNA expression of EPHX2 was significantly downregulated in the majority of tumors compared with normal tissues. Despite the significant prognostic value of EPHX2 expression across cancers, EPHX2 played a protective or detrimental role in different kinds of cancers. Generally speaking, immune cell infiltrations, immune modulators and immunotherapeutic biomarkers were all strongly related to the expression of EPHX2. Besides, EPHX2 expression was significantly related to immune-relevant pathways, especially in PAAD, THYM and UVM. Furthermore, our study demonstrated diverse response patterns of ICB in response to EPHX2 expression in different tumor types. Conclusion: Our findings here suggest that EPHX2 could be a prognostic factor in multiple cancers and play an important role in tumor immunity by affecting infiltrating immune cells, TMB and MSI. This study provides further insight into the role of EPHX2 in tumor immunotherapy.
Senescence is a double-edged sword in tumorigenesis and affects the immunotherapy response through the modulation of the host’s immune system. However, there is currently a lack of comprehensive analysis of the senescence-related genes (SRGs) in human cancers, and the predictive role of senescence in cancer immunotherapy response has not been explored. The multi-omics approaches were performed in this article to conduct a systematic pan-cancer genomic analysis of SRGs in cancer. In addition, we calculated the generic senescence score (SS) to quantify the senescence levels in cancers and explored the correlations of SS with cancer prognosis, biological processes, and tumor microenvironment (TME). The gene signatures were deregulated in multiple cancers and indicated a context-dependent correlation with prognosis, tumor-immune evasion, and response to therapy across various tumor types. Further analysis disclosed that SS was positively associated with the infiltration levels of immune suppressive cells, including induced Tregs (iTregs), central memory Ts (Tcms), and natural Tregs (nTregs), and negatively associated with immune killer cells, including natural killers (NKs) and mucosal-associated invariant Ts (MAITs). Moreover, the SS was significantly correlated with tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), immune-related genes, and immune checkpoints and had a predictive value of immunotherapy response. Thus, the expression of SRGs was involved in resistance to several anticancer drugs. Our work illustrates the characterization of senescence across various malignancies and highlights the potential of senescence as a biomarker of the response to immunotherapy.
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