Although the deregulation of lysine methyltransferase (su(var)-3–9, enhancer-of-zeste, trithorax) domain-containing protein 7/9 (SET7/9) has been identified in a variety of cancers, the potential role of SET7/9 and the molecular events in which it is involved in breast cancer remain obscure. Using the online Human Protein Atlas and GEO databases, the expression of SET7/9 was analyzed. Furthermore, we investigated the underlying mechanisms using chromatin immunoprecipitation-based deep sequencing (ChIP-seq) and quantitative ChIP assays. To explore the physiological role of SET7/9, functional analyses such as CCK-8, colony formation, and transwell assays were performed and a xenograft tumor model was generated with the human breast cancer cell lines MCF-7 and MDA-MB-231. Mass spectrometry, co-immunoprecipitation, GST pull-down, and ubiquitination assays were used to explore the mechanisms of SET7/9 function in breast cancer. We evaluated the expression of SET7/9 in different breast cancer cohorts and found that higher expression indicated worse survival times in these public databases. We demonstrated positive effects of SET7/9 on cell proliferation, migration, and invasion via the activation of Runt-related transcription factor 2 (RUNX2). We demonstrate that tripartite motif-containing protein 21 (TRIM21) physically associates with SET7/9 and functions as a major negative regulator upstream of SET7/9 through a proteasome-dependent mechanism and increased ubiquitination. Taken together, our data suggest that SET7/9 has a promoting role via the regulation of RUNX2, whereas TRIM21-mediated SET7/9 degradation acts as an anti-braking system in the progression of breast cancer.

Zinc-figure protein 217 (ZNF217) is a C2H2 zinc finger transcription factor that works as a pivotal effector stimulating embryonic immortalization as well as oncogenicity during multiple cancer processes. Nevertheless, the expression of ZNF217 in hepatocellular carcinoma (HCC) and the underlying specific molecular mechanisms remains elusive. In the present study, we aimed to explore the potential role of ZNF217 in HCC cell proliferation and invasion, as well as the underlying mechanism. Here, we demonstrated that the expression of ZNF217 was higher in HCC patients and indicated worse overall survival times, which was confirmed by Oncomine datasets and The Cancer Genome Atlas (TCGA) HCC cohorts. Further research discovered that knockdown of ZNF217 inhibited the proliferation of HCC cells in vitro and in vivo. Enforced expression of ZNF217 could promote Epithelial-mesenchymal transition and thus the invasion of HCC cells. Mechanistically, we identified ZNF217 interacted with LSD1 in vivo and in vitro. Knockdown of ZNF217 was accompanied by a parallel increase in di-methyl histone 3 lysine4 levels on CDH1 promoter, which indicated ZNF217 could recruit LSD1 to affect CDH1 epigenetic expression from transcription level. Of note, bioinformatics analyses, a dual luciferase reporter assay, RT-qPCR and western blot analysis demonstrated that microRNA-101 (miR-101), a well-known tumor suppressor in HCC, acted as a negative regulator of ZNF217. The inhibition of HCC progression by miR-101 was counteracted by ZNF217 overexpression. Taken together, our study presents the regulation mechanism of miR-101/ZNF217/CDH1 axis for the first time and provides new evidences of ZNF217 as a potential therapeutic target for HCC patients.

Rapid, high-throughput, timely, multiplex diagnosis of respiratory-tract infections still relies on laboratory infrastructure, sequential assays, and trained personnel, thereby delaying targeted therapy and outbreak containment. In this study, a Fully Automated rotary microfluidic platform (FA-RMP) for high-throughput multiplex respiratory tract pathogens detection was presented. FA-RMP enables a true “sample-in, result-out” workflow through the integration of swab lysis, reagent partitioning, lyophilized reverse transcription loop-mediated isothermal amplification (RT-LAMP), and moving-probe fluorescence read-out, all encapsulated with a disposable microfluidic cartridge and paired with a 9 kg, four-channel benchtop reader. The FA-RMP enables parallel processing of 16 independent reactions within 30 min, supporting simultaneous detection of up to 4 distinct clinical samples. Analytical validation using serially diluted Mycoplasma pneumoniae (MP) DNA established a limit of detection (LoD) of 50 copies µL⁻¹ and a log-linear correlation between threshold time and template load (R² = 0.9528). Testing with eight non-target respiratory pathogens yielded no amplification, confirming high analytical specificity. FA-RMP successfully detected the clinical samples with influenza A, influenza B, and MP, further demonstrating its robust multiplex detection capability. By integrating automated sample preparation, multiplex isothermal amplification and quantitative detection into a portable, high-throughput system, the platform delivers laboratory-grade performance at the point of care, serving as a scalable tool for routine respiratory pathogens screening and rapid epidemic response.

Epigenetic modifications, particularly RNA methylation, play a crucial role in cancer progression, and N6-methyladenosine (m6A) is the most prevalent mRNA modification in eukaryotes. Wilms tumor 1-associated protein (WTAP), a key component of the m6A methyltransferase complex (MTC), regulates m6A modification, influencing RNA stability, translation, and degradation. WTAP dysregulation has been implicated in various malignancies, with particularly significant roles observed across the digestive system cancers, including but not limited to esophageal, gastric, pancreatic, gallbladder, hepatocellular, and colorectal carcinomas. Overexpression of WTAP is frequently associated with poor prognosis, advanced tumor stages, and increased metastatic potential. This review highlights the multifaceted roles and regulatory network of WTAP in digestive system cancers (DSCs) progression, encompassing tumor cell proliferation, migration, invasion, drug resistance, and immune evasion. Targeting WTAP may offer novel therapeutic strategies for overcoming therapy resistance and improving clinical outcomes in digestive system malignancies. Future research should prioritize: (1) validation of these findings in larger, multicenter, and ethnically diverse patient cohorts; (2) comprehensive elucidation of the molecular mechanisms underlying WTAP-mediated regulation in cancer biology; and (3) systematic exploration of its functional consequences in tumor progression and therapy resistance.

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, a status primarily attributable to its intricate molecular circuitry. The histone acylation network serves as a key orchestrator of PDAC progression through epigenetic reprogramming, making its regulatory components high-value targets for groundbreaking therapeutic interventions. Here, we review how diverse histone acylations govern pancreatic cancer biology. We first outline the established roles of acetylation in proliferation, metastasis, and immune evasion. Subsequently, we focus on novel modifications intimately linked to tumor metabolic reprogramming, with a particular emphasis on histone lactylation. We also explore emerging modifications such as succinylation and propionylation as potential therapeutic targets. We further underscore that these diverse acylations exhibit extensive crosstalk, forming an intricate and dynamic regulatory network mediated by shared enzymatic “writers” and “erasers” (e.g., p300, HDACs), and exerting synergistic or antagonistic effects on key genes including MYC and GATA binding protein 6 (GATA6). By providing a comprehensive deciphering of the dysregulated histone acylation network, this review highlights its significant transformative potential. Such understanding not only unveils novel pathogenic drivers of pancreatic tumorigenesis but also establishes a mechanistic foundation for precision oncology. Furthermore, we evaluate the current landscape of clinical trials and discuss the potential of epigenetic agents to sensitize tumors to conventional or targeted therapies. By bridging the gap between complex molecular crosstalk and clinical application, this review aims to provide a practical framework for the rational design of targeted inhibitors and the formulation of synergistic combination therapies to overcome current treatment limitations and therapeutic resistance.