Recently, the US Food and Drug Administration (FDA) approved the first chimeric antigen receptor T cell (CAR-T) therapy for the treatment CD19-positive B cell acute lymphoblastic leukemia. While CAR-T has achieved remarkable success in the treatment of hematopoietic malignancies, whether it can benefit solid tumor patients to the same extent is still uncertain. Even though hundreds of clinical trials are undergoing exploring a variety of tumor-associated antigens (TAA), no such antigen with comparable properties like CD19 has yet been identified regarding solid tumors CAR-T immunotherapy. Inefficient T cell trafficking, immunosuppressive tumor microenvironment, suboptimal antigen recognition specificity, and lack of safety control are currently considered as the main obstacles in solid tumor CAR-T therapy. Here, we reviewed the solid tumor CAR-T clinical trials, emphasizing the studies with published results. We further discussed the challenges that CAR-T is facing for solid tumor treatment and proposed potential strategies to improve the efficacy of CAR-T as promising immunotherapy.

Medicinal plants are important sources of bioactive specialized metabolites with significant therapeutic potential. Advances in multi-omics have accelerated the understanding of specialized metabolite biosynthesis and regulation. Genomics, transcriptomics, proteomics, and metabolomics have each contributed new insights into biosynthetic gene clusters (BGCs), metabolic pathways, and stress responses. However, single-omics approaches often fail to fully address these complex processes. Integrated multi-omics provides a holistic perspective on key regulatory networks. High-throughput sequencing and emerging technologies like single-cell and spatial omics have deepened our understanding of cell-specific and spatially resolved biosynthetic dynamics. Despite these advancements, challenges remain in managing large datasets, standardizing protocols, accounting for the dynamic nature of specialized metabolism, and effectively applying synthetic biology for sustainable specialized metabolite production. This review highlights recent progress in omics-based research on medicinal plants, discusses available bioinformatics tools, and explores future research trends aimed at leveraging integrated multi-omics to improve the medicinal quality and sustainable utilization of plant resources.

Acetaminophen (APAP) is a widely used analgesic and antipyretic over-the-counter medicine worldwide. Hepatotoxicity caused by APAP overdose is one of the leading causes of acute liver failure (ALF) in the US and in some parts of Europe, limiting its clinical application. Excessive APAP metabolism depletes glutathione and increases N-acetyl-p-benzoquinoneimide (NAPQI) levels, leading to oxidative stress, DNA damage, and cell necrosis in the liver, which in turn leads to liver damage. Studies have shown that natural products such as polyphenols, terpenes, anthraquinones, and sulforaphane can activate the hepatocyte antioxidant defense system with Nrf2 as the core player, reduce oxidative stress damage, and protect the liver. As the key enzyme metabolizing APAP into NAPQI, cytochrome P450 enzymes are also considered to be intriguing target for the treatment of APAP-induced liver injury. Here, we systematically review the hepatoprotective activity and molecular mechanisms of the natural products that are found to counteract the hepatotoxicity caused by APAP, providing reference information for future preclinical and clinical trials of such natural products.

Plants can suffer ammonium (NH4 +) toxicity, particularly when NH4 + is supplied as the sole nitrogen source. However, our knowledge about the underlying mechanisms of NH4 + toxicity is still largely unknown. Lemna minor, a model duckweed species, can grow well in high NH4 + environment but to some extent can also suffer toxic effects. The transcriptomic and physiological analysis of L. minor responding to high NH4 + may provide us some interesting and useful information not only in toxic processes, but also in tolerance mechanisms. The L. minor cultured in the Hoagland solution were used as the control (NC), and in two NH4 + concentrations (NH4 + was the sole nitrogen source), 84 mg/L (A84) and 840 mg/L (A840) were used as stress treatments. The NH4 + toxicity could inhibit the growth of L. minor. Reactive oxygen species (ROS) and cell death were studied using stained fronds under toxic levels of NH4 +. The malondialdehyde content and the activities of superoxide dismutase and peroxidase increased from NC to A840, rather than catalase and ascorbate peroxidase. A total of 6.62G nucleotides were generated from the three distinct libraries. A total of 14,207 differentially expressed genes (DEGs) among 70,728 unigenes were obtained. All the DEGs could be clustered into 7 profiles. Most DEGs were down-regulated under NH4 + toxicity. The genes required for lignin biosynthesis in phenylpropanoid biosynthesis pathway were up-regulated. ROS oxidative-related genes and programmed cell death (PCD)-related genes were also analyzed and indicated oxidative damage and PCD occurring under NH4 + toxicity. The first large transcriptome study in L. minor responses to NH4 + toxicity was reported in this work. NH4 + toxicity could induce ROS accumulation that causes oxidative damage and thus induce cell death in L. minor. The antioxidant enzyme system was activated under NH4 + toxicity for ROS scavenging. The phenylpropanoid pathway was stimulated under NH4 + toxicity. The increased lignin biosynthesis might play an important role in NH4 + toxicity resistance.