Cryptotanshinone (IUPAC name: (R)-1,2,6,7,8,9-hexahydro-1,6,6-trimethyl-phenanthro(1,2-b)furan-10,11-dione), a biologically active constituent extracted from the roots and rhizomes of the plant Salvia miltiorrhiza, has been studied in depth as a medicinally active compound and shown to have efficacy in the treatment of numerous diseases and disorders. In this review, we describe in detail the current status of cryptotanshinone research, including findings relating to the structure, pharmacokinetics, pharmacological activity, and derivatives of this compound. Cryptotanshinoneh as a diverse range of pharmacological effects, including anti-cancer, anti-inflammatory, immune regulatory, neuroprotective, and anti-fibrosis activities. Studies on the molecular mechanisms underlying the activities of cryptotanshinone have established that the JAK2/STAT3, PI3K/AKT, NF-κB, AMPK, and cell cycle pathways are involved in the inhibitory and pro-apoptotic effects of cryptotanshinone on different tumor cell lines, these molecular pathways interact in a coordinated manner to inhibit cell proliferation, migration and invasion,and induce transformation, autophagy, necrosis, and cellular immunity. The anti-inflammatory mechanisms of cryptotanshinone have been found to be associated with the TLR4-MyD88/PI3K/Nrf2 and TLR4-MyD88/NF-κB/MAPK pathways, whereasthe Hedgehog, NF-κB, and Nrf-2/HO-1 pathways are regulated by cryptotanshinone to reduce organ fibrosis, and its inhibitory effects on the PI3K/AKT-eNOS pathway have been linked to neuroprotective effects. Given the potential medicinal utility of cryptotanshinone, further research is needed to verify the efficacy and safety of this compound in clinical use, evaluate its pharmacological activity, and identify molecular targets.

Background: Studies have shown that long noncoding RNAs (lncRNAs) make up the major proportion of the ceRNA network and can regulate gene expression by competitively binding to miRNAs. This reveals the existence of an RNA-miRNA regulatory pathway and is of great biological significance. CeRNAs, as competitive endogenous RNAs, have revealed a new mechanism of interaction between RNAs. Until now, the role of lncRNA-mediated ceRNAs in breast cancer and their regulatory mechanisms have been elucidated to some extent. Purpose: In this study, comprehensive analysis of large-scale invasive breast cancer samples in TCGA were conducted to further explore the developmental mechanism of invasive breast cancer and the potential predictive markers for invasive breast cancer prognosis in the ceRNA network. Methods: Abnormal expression profiles of invasive breast cancer associated mRNAs, lncRNAs and miRNAs were obtained from the TCGA database. Through further alignment and prediction of target genes, an abnormal lncRNA-miRNA-mRNA ceRNA network was constructed for invasive breast cancer. Through the overall survival analysis, Identification prognostic biomarkers for invasive breast cancer patients，In addition, we used Cytoscape plug-in BinGo for the different mRNA performance functional cluster analysis. Results: Differential analysis revealed that 1059 lncRNAs, 86 miRNAs, and 2138 mRNAs were significantly different in invasive breast cancer samples versus normal samples. Then we construct an abnormal lncRNA-miRNA-mRNA ceRNA network for invasive breast cancer, consisting of 90 DElncRNAs, 18 DEmiRNAs and 26 DEmRNAs.Further, 4 out of 90 lncRNAs, 3 out of 26 mRNAs, and 2 out of 18 miRNAs were useful as prognostic biomarkers for invasive breast cancer patients (P value < 0.05). It is worth noting that based on the ceRNA network, we found that the LINC00466-Hsa-mir-204- NTRK2 LINC00466-hsa-mir-204-NTRK2 axis was present in 9 RNAs associated with the prognosis of invasive breast cancer.
Conclusion: This study provides an effective bioinformatics basis for further understanding of the molecular mechanism of invasive breast cancerand for predicting outcomes, which can guide the use of invasive breast cancerdrugs and subsequent related research.

Innate immune mechanisms initiate immune responses via pattern-recognition receptors (PRRs). Cyclic GMP-AMP synthase (cGAS), a member of the PRRs, senses diverse pathogenic or endogenous DNA and activates innate immune signaling pathways, including the expression of stimulator of interferon genes (STING), type I interferon, and other inflammatory cytokines, which, in turn, instructs the adaptive immune response development. This groundbreaking discovery has rapidly advanced research on host defense, cancer biology, and autoimmune disorders. Since cGAS/STING has enormous potential in eliciting an innate immune response, understanding its functional regulation is critical. As the most widespread and efficient regulatory mode of the cGAS-STING pathway, post-translational modifications (PTMs), such as the covalent linkage of functional groups to amino acid chains, are generally considered a regulatory mechanism for protein destruction or renewal. In this review, we discuss cGAS-STING signaling transduction and its mechanism in related diseases and focus on the current different regulatory modalities of PTMs in the control of the cGAS-STING-triggered innate immune and inflammatory responses.

As one of the most common malignant tumors in humans, lung cancer has experienced a gradual increase in morbidity and mortality. This study examined prognosis-related methylation-driven genes specific to lung adenocarcinoma (LUAD) to provide a basis for prognosis prediction and personalized targeted therapy for LUAD patients. The methylation and survival time data from LUAD patients in the TCGA database were downloaded. The MethylMix algorithm was used to identify the differential methylation status of LUAD and adjacent tissues based on the β-mixture model to obtain disease-related methylation-driven genes. A COX regression model was then used to screen for LUAD prognosis-related methylation-driven genes, and a linear risk model based on five methylation-driven gene expression profiles was constructed. A methylation and gene expression combined survival analysis was performed to further explore the prognostic value of 5 genes independently. There were 118 differentially expressed methylation-driven genes in the LUAD tissues and adjacent tissues. Five of the genes, CCDC181, PLAU, S1PR1, ELF3, and KLHDC9, were used to construct a prognostic risk model. Overall, the survival time was significantly lower in the high-risk group compared with that in the low-risk group (P < 0.05). In addition, the methylation and gene expression combined survival analysis found that the combined expression levels of the genes CCDC181, PLAU, and S1PR1 as well as KLHDC9 alone can be used as independent prognostic markers or drug targets. Our findings provide an important bioinformatic basis and relevant theoretical basis for guiding subsequent LUAD early diagnosis and prognosis assessments.

Danshen (Salvia miltiorrhiza Bunge), a natural powerful drug for various conditions treatment, has traditionally been used in Asian countries for centuries as anticancer agent, anti‐inflammatory agent, and antioxidant. More recently, it is explored in combination with other herbs for skeletal diseases therapy; bone‐targeting compounds with pharmacological activities have been isolated from various sources of traditional Chinese medicine (TCM), including Danshen. In this case, some evidence supports that Danshen may treat myelofibrosis (MF) by exerting its antitumor effect. To study the specific mechanism of Danshen in the treatment of MF, we used bioinformatics databases to determine its active ingredients. Then, identification of target proteins related to MF was made using a network pharmacology analysis platform. In our results, 20 key active compounds and 457 key targets of Danshen were identified. In‐depth network analysis of the top diseases, functions, and pathways suggested that a common underlying mechanism linked Danshen involvement with MF. Finally, 5 potential targets were confirmed by the analysis; these 5 targets, as well as 20 previously identified compounds, were subjected to molecular docking experiments. The results indicated that cryptotanshinone of Danshen may affect MF by acting on the key genes in the JAK‐STAT signalling pathway and the TGF‐β signalling pathway.