Laccase belongs to the superfamily of multicopper oxidases and has been widely investigated in recent decades. Due to its mild and efficient oxidation of substrates, laccase has been successfully applied in organic catalytic synthesis, the degradation of harmful substances, and other green catalytic fields. Nevertheless, there are few reports on the green catalysis with laccase. This review focuses on reporting and collating some of the latest interesting laccase-catalyzed bond formation and breakage research. This is discussed with a focus on the effects of the medium system on the laccase-catalyzed reaction, as well as the formation and the breakage of C–N, C–C, and C–O bonds catalyzed by laccase. It provides abundant references and novel insights for furthering the industrial applications of laccase.

Reactive oxygen species (ROS) encompasses a collection of complicated chemical entities characterized by individually specific biological reactivities and physicochemical properties. ROS detection is attracting tremendous attention. The reaction-based nanomaterials for ROS “turn-on” sensing represent novel and efficient tools for ROS detection. These nanomaterials have the advantages of high sensitivity, real-time sensing ability, and almost infinite contrast against background. This review focuses on appraising nanotechnologies with the ROS “turn-on” detection mechanism coupled with the ability for broad biological applications. In this review, we highlighted the weaknesses and advantages in prior sensor studies and raised some guidelines for the development of future nanoprobes.

Nitroreductase activable agents offer a personalized and targeted approach to cancer theranostics by selectively activating prodrugs within the tumor microenvironment. These agents enable non-invasive tumor imaging, image-guided drug delivery, and real-time treatment monitoring. By leveraging the enzymatic action of tumor-specific nitroreductase enzymes, cytotoxic drugs are delivered directly to cancer cells while minimizing systemic toxicity. This review highlights the key features, mechanisms of action, diagnostic applications, therapeutic potentials, and future directions of nitroreductase activable agents for tumor theranostics. Integration with imaging modalities, advanced drug delivery systems, immunotherapy combinations, and theranostic biomarkers shows promise for optimizing treatment outcomes and improving patient survival in oncology. Continued research and innovation in this field are crucial for advancing novel theranostic strategies and enhancing patient care. Nitroreductase activable agents represent a promising avenue for personalized cancer therapy and have the potential to transform cancer diagnosis and treatment approaches.

Cancer immunotherapy has revolutionized the treatment of various malignancies, particularly with the advent of immune checkpoint inhibitors and CAR-T cell therapies [1][2][3]. These approaches have yielded impressive outcomes in a subset of patients, yet many still fail to achieve durable responses [4]. One of the key reasons for this disparity in treatment outcomes is the presence of an immunosuppressive tumor microenvironment (TME), which plays a crucial role in limiting the effectiveness of immune-based therapies [5,6]. The TME comprises a complex network of cellular and molecular components, including tumor-associated macrophages (TAMs), regulatory T cells (Tregs), and myeloid-derived suppressor cells (MDSCs), all of which contribute to immune evasion and tumor progression [7][8][9].The STING (stimulator of interferon genes) pathway has emerged as a promising target for cancer immunotherapy due to its ability to bridge innate and adaptive immune responses [10,11]. Upon activation by cytosolic DNA, the STING pathway triggers the production of type I interferons and other pro-inflammatory cytokines, leading to the activation of dendritic cells (DCs) and subsequent priming of T cells [12]. This process is crucial for initiating a robust anti-tumor immune response.However, despite the potential of STING agonists to stimulate powerful immune responses, their efficacy in clinical settings has been limited, primarily due to the immunosuppressive nature of the TME, which can dampen the immune activation initiated by STING [13]. This TME comprises various cellular components, including TAMs, regulatory Tregs, and MDSCs, which together contribute to a hostile immune environment that inhibits effective anti-tumor responses.TAMs often adopt an M2-like phenotype within the TME, characterized by anti-inflammatory and tissue-remodeling activities that promote tumor growth and suppress effective immune responses [14]. Recent studies have shown that activation of the STING pathway can lead to a shift in TAM polarization from M2 to M1, enhancing the secretion of pro-inflammatory cytokines such as TNF-α and IL-12, which are crucial for T cell activation and anti-tumor immunity. Tregs play a dual role in maintaining immune homeostasis but can hinder effective anti-tumor immunity by inhibiting cytotoxic T cell functions. Targeting Tregs through STING agonists may lead to a decrease in their suppressive effects, allowing for a more robust T cell response against tumor cells [15].MDSCs represent a significant barrier to successful immunotherapy due to their ability to produce reactive oxygen species (ROS) and other immunosuppressive factors that inhibit T cell activation.Emerging evidence suggests that STING agonists may reduce MDSC levels or impair their function, thereby alleviating the suppression of T cell activity within the TME [16,17]. The extracellular matrix (ECM) and the physical characteristics of the TME, such as hypoxia and acidosis, also contribute to immune suppression. STING activation can enhance the remodeling of the ECM, thereby facilitating better immune cell infiltration and improving the therapeutic efficacy of STING agonists [18].Given these challenges, there is a growing interest in exploring synergistic combination strategies that not only modulate the TME but also enhance the overall effectiveness of STING agonists [19,20]. For instance, targeting specific components of the TME that contribute to immune suppression, such as TAMs, regulatory Tregs, and MDSCs, can create a more favorable environment for STING-mediated immune activation [21,22]. Recent studies have demonstrated that combining STING agonists with therapies like checkpoint inhibitors or bispecific antibodies leads to enhanced T cell responses and improved tumor regression. This synergistic approach has shown great promise not only in improving the efficacy of STING agonists but also in overcoming resistance mechanisms associated with current immunotherapies. By leveraging multiple therapeutic modalities, researchers aim to achieve more durable and effective anti-tumor responses, ultimately leading to better patient outcomes [23]. This article will delve into the characteristics of the TME, the role of the STING pathway in tumor immunotherapy, and how combining TME modulation with STING agonists can lead to more effective cancer treatments. This article uniquely contributes to the field by systematically evaluating the synergistic potential of STING agonists combined with TME-modulating therapies, which is often overlooked in current literature. Moreover, it emphasizes the critical need for personalized therapeutic strategies that consider the distinct characteristics of individual tumor microenvironments, thereby optimizing treatment efficacy. Additionally, the manuscript outlines future research directions that aim to elucidate the specific mechanisms by which STING pathway activation interacts with various TME components, paving the way for innovative clinical applications. Unlike previous studies that primarily focus on isolated therapeutic interventions, this manuscript provides a comprehensive overview of how the combination of STING agonists with diverse TME-targeting strategies can significantly optimize the immune response and improve patient outcomes.TME is a complex and dynamic entity that plays a critical role in tumor progression and the response to cancer therapies [24,25]. It consists of various cellular components, including cancer cells, immune cells, fibroblasts, endothelial cells, and ECM components [26]. Among the immune cells, TAMs, regulatory Tregs, and MDSCs are key players that contribute to the immunosuppressive nature of the TME [7][8][9].TAMs often adopt an M2-like phenotype within the TME, characterized by anti-inflammatory and tissue-remodeling activities that promote tumor growth and suppress effective immune responses [27]. These cells secrete cytokines such as IL-10 and...