Lei Xia

Sepsis has a high morbidity and mortality rate, and effective therapeutic options remain limited. Lipopolysaccharide (LPS) is known to induce significant changes in the expression of forkhead box O (FOXO) transcription factor family members, and the mechanisms by which various drugs, including dexamethasone, treat sepsis are associated with the FOXO signaling pathway. Increased FOXO3 expression can reduce levels of inflammatory mediators, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), by more than one-third. However, FOXO proteins not only regulate inflammatory activity but also function as transcription factors with important roles across various tissues. The FOXO transcription factor family participates in cell-cycle regulation, apoptosis, autophagy, stress responses, DNA repair, tumorigenesis, and metabolism. Current research shows that FOXO proteins affect the occurrence, progression, and prognosis of sepsis by regulating several processes, including pro- and anti-inflammatory responses, immune regulation, oxidative stress, mitochondrial activity, vascular injury, and gut microbiota translocation. With improved understanding of FOXO-related mechanisms, researchers have proposed several strategies for therapeutic development targeting FOXO. These approaches include targeting upstream post-translational modifications, designing small-molecule agents that act on FOXO, regulating downstream proteins, and applying multi-target intervention strategies. These directions offer new possibilities for sepsis treatment.

Vitexin (apigenin-8-C-beta-D-glucopyranoside) is a natural flavonoid derivative with anti-cancer, antioxidant, anti-inflammatory, antihypertensive, anti-asthma, anti-epilepsy, and other therapeutic effects. It is extracted from pearl millet, hawthorn, pigeon bean, mung bean, and other medicinal plants. Vitexin has received widespread attention because of its significant anti-tumor effect. It induces apoptosis and anti-tumor angiogenesis, inhibits tumor cell migration and invasion, regulates tumor cell autophagy and immunity, and increases patient sensitivity to radiotherapy and chemotherapy. It has a significant anti-tumor effect on breast, prostate, liver, cervical, and colon cancers, gliomas, and other malignant tumors. This review demonstrates the latest research progress on the anti-tumor effects and potential mechanisms of vitexin. It summarizes its anti-tumor mechanism to provide new theoretical support and reference for cancer treatment.

Background: The role of drug repositioning in the treatment of ovarian cancer has received increasing attention. Although promising results have been achieved, there are also major controversies.Methods: In this study, we conducted a drug-target Mendelian randomisation (MR) analysis to systematically investigate the reported effects and relevance of traditional drugs in the treatment of ovarian cancer. The inverse-variance weighted (IVW) method was used in the main analysis to estimate the causal effect. Several MR methods were used simultaneously to test the robustness of the results.Results: By screening 31 drugs with 110 targets, FNTA, HSPA5, NEU1, CCND1, CASP1, CASP3 were negatively correlated with ovarian cancer, and HMGCR, PLA2G4A, ITGAL, PTGS1, FNTB were positively correlated with ovarian cancer.Conclusion: Statins (HMGCR blockers), lonafarnib (farnesyltransferase inhibitors), the anti-inflammatory drug aspirin, and the anti-malarial drug adiponectin all have potential therapeutic roles in ovarian cancer treatment.

Ginger is a common aromatic vegetable with a wide range of functional ingredients and considerable medicinal and nutritional properties. Numerous studies have shown that ginger and its active ingredients have suppressive effects on manifold tumours, including ovarian cancer (OC). However, the molecular mechanism by which ginger inhibits OC is not clear. The aim of this study was to investigate the function and mechanism of ginger in OC. The estimation of n6-methyladenosine (m6A) levels was performed using the m6A RNA Methylation Quantification Kit, and RT-qPCR was used to determine the expression of m6A-related genes and proteins. The m6A methylationome was detected by MeRIP-seq, following analysis of the data. Differential methylation of genes was assessed utilizing RT-qPCR and Western Blotting. The effect of ginger on SKOV3 invasion in ovarian cancer cells was investigated using the wound healing assay and transwell assays. Ginger significantly reduced the m6A level of OC cells SKOV3. The 3’UTR region is the major site of modification for m6A methylation, and its key molecular activities include Cell Adhesion Molecules, according to meRIP-seq results. Moreover, it was observed that Ginger aids significantly in downregulating the CLDN7, CLDN11 mRNA, and protein expression. The results of wound healing assay and transwell assay showed that ginger significantly inhibited the invasion of OC cells SKOV3. Ginger inhibits ovarian cancer cells’ SKOV3 invasion by regulating m6A methylation through CLDN7, CLDN11, and CD274.

N6-methyladenosine (m6A) modification is a class of epitope modifications that has received significant attention in recent years, particularly in relation to its role in various diseases, including sepsis. Epigenetic research has increasingly focused on m6A modifications, which is influenced by the dynamic regulation of three protein types: ‟Writers” (such as METTL3/METTL14/WTAP)—responsible for m6A modification; ‟Erasers” (FTO and ALKBH5)—involved in m6A de-modification; and ‟Readers” (YTHDC1/2, YTHDF1/2/3)—responsible for m6A recognition. Sepsis, a severe and fatal infectious disease, has garnered attention regarding the crucial effect of m6A modifications on its development. In this review, we attempted to summarize the recent studies on the involvement of m6A and its regulators in sepsis, as well as the significance of m6A modifications and their regulators in the development of novel drugs and clinical treatment. The potential value of m6A modifications and modulators in the diagnosis, treatment, and prognosis of sepsis has also been discussed. Graphical abstract

Saffron is located in the upper part of the crocus stigma of iridaceae, which has a long history of medicinal use. Crocin (molecular formula C₄₄H₆₄O₂₄) is a natural floral glycoside ester compound extracted from saffron, which is a type carotenoid. Modern pharmacological studies have shown that crocin has multiple therapeutic effects including anti-inflammatory, anti-oxidant, anti-hyperlipidemic and anti-stone effects. In recent years, crocin has been widely noticed due to its considerable anti-tumor effects manifested by the induction of tumor cell apoptosis, inhibition of tumor cell proliferation, inhibition of tumor cell invasion and metastasis, enhancement of chemotherapy sensitivity and improvement of immune status. The anti-tumor effects have been shown in various malignant tumors such as gastric cancer, liver cancer, cervical cancer, breast cancer and colorectal cancer. In this review, we compiled recent studies on the anti-tumor effects of crocin and summarized its anti-tumor mechanism for developing ideas of treating malignancies and exploring anti-tumor drugs.

Cancer is a significant disease that poses a major threat to human health. The main therapeutic methods for cancer include traditional surgery, radiotherapy, chemotherapy, and new therapeutic methods such as targeted therapy and immunotherapy, which have been developed rapidly in recent years. Recently, the tumor antitumor effects of the active ingredients of natural plants have attracted extensive attention. Ferulic acid (FA), (3-methoxy-4-hydroxyl cinnamic), with the molecular formula is C₁₀H₁₀O₄, is a phenolic organic compound found in ferulic, angelica, jujube kernel, and other Chinese medicinal plants but is also, abundant in rice bran, wheat bran, and other food raw materials. FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity, as it can inhibit the occurrence and development of various malignant tumors, such as liver cancer, lung cancer, colon cancer, and breast cancer. FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS). FA can also interfere with the cell cycle of cancer cells, arrest most cancer cells in G₀/G₁ phase, and exert an antitumor effect by inducing autophagy; inhibiting cell migration, invasion, and angiogenesis; and synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions. FA acts on a series of intracellular and extracellular targets and is involved in the regulation of tumor cell signaling pathways, including the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT), B-cell lymphoma-2 (Bcl-2), and tumor protein 53 (P53) pathways and other signaling pathways. In addition, FA derivatives and nanoliposomes, as platforms for drug delivery, have an important regulatory effect on tumor resistance. This paper reviews the effects and mechanisms of antitumor therapies to provide new theoretical support and insight for clinical antitumor therapy.