The diagnosis of hepatic precancerous lesions (HPC) and early hepatocellular carcinoma (HCC) has significant public health implications and holds the potential to reduce the global burden of HCC. This study aimed to identify molecular features and biomarkers associated with HPC progression and early HCC development.

RNA sequencing was used to identify differentially expressed genes in mouse HPC tissues and normal liver tissues. Cyclin E1 (CCNE1) expression in HPC tissues and HCC cells was assessed using immunohistochemistry, Western blotting, and real-time polymerase chain reaction. The effects of CCNE1 on HCC cell proliferation, migration, invasion, and apoptosis were evaluated using colony formation, wound healing, Transwell assays, and flow cytometry. The mechanism of CCNE1 was explored through Kyoto Encyclopedia of Genes and Genomes pathway analysis and gene set enrichment analysis and further validated through in vitro experiments. The interaction between CCNE1 and tumor-associated macrophages (TAMs) was investigated by co-culturing HCC cells with macrophages.

RNA sequencing and TCGA database analysis showed that CCNE1 expression was significantly elevated in mouse HPC tissues and human HCC samples and was associated with reduced survival rates. In vitro assays demonstrated that CCNE1 promoted HCC cell proliferation, migration, invasion, and survival by activating the PI3K/Akt signaling pathway. Additionally, CCNE1 induced TAM polarization toward the M2 phenotype by promoting the expression of CCL2 and CCL5 in HCC cells.

CCNE1 promotes HPC progression and HCC cell proliferation, migration, invasion, and survival by activating the PI3K/Akt signaling pathway. Furthermore, CCNE1 enhances the secretion of CCL2 and CCL5 by HCC cells, promoting TAM infiltration and M2 polarization, thereby contributing to tumor progression.

Ferroptosis plays an essential role in chronic liver diseases, and cyclooxygenase-2 (COX-2) affects liver fibrosis through multiple mechanisms. However, research on COX-2 regulation of ferroptosis in chronic liver injury remains limited. This study aimed to investigate whether and how COX-2 regulates ferroptosis in chronic liver injury.

In vivo, a thioacetamide (TAA)-induced chronic liver injury model, characterized by significant liver lipid peroxidation and oxidative stress, was used. COX-2+/+ and COX-2–/– mice were treated with TAA or normal saline. In vitro, primary mouse hepatocytes were isolated and treated with dimethyl sulfoxide (DMSO), erastin+DMSO, etoricoxib+erastin+DMSO, and tBHQ+erastin+DMSO. Mitochondrial morphology, iron metabolism, lipid peroxidation, and oxidative stress were assessed to verify ferroptosis. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway was measured to investigate the relationship between COX-2 and ferroptosis.

TAA-treated COX-2–/– mice presented milder liver fibrosis, whereas TAA-treated COX-2–/– mice livers and etoricoxib+erastin+DMSO-treated primary hepatocytes exhibited alleviated mitochondrial damage compared with TAA-treated COX-2+/+ littermates and erastin+DMSO-treated primary hepatocytes, respectively. The knockout of COX-2 decreased ferrous ion concentration (p < 0.01) and mitigated lipid peroxidation in TAA-treated livers (p < 0.05). Furthermore, both COX-2 knockout and etoricoxib restored reduced glutathione (p < 0.05) and glutathione peroxidase 4 (p < 0.05), while decreasing malondialdehyde levels (p < 0.05). Additionally, COX-2 inhibition upregulated Nrf2, which helped alleviate erastin+DMSO-induced ferroptosis (p < 0.01).

Ferroptosis contributes to the progression of chronic liver injury. Inhibition of COX-2 upregulates Nrf2, mitigating hepatocyte ferroptosis in chronic liver injury.

General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating cell proliferation. However, the role of GTF3C2 in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine its expression, biological function, and mechanism in HCC.

The expression of GTF3C2 in HCC and non-tumor tissues, along with its clinical significance, was investigated using public databases and clinical samples. Reverse transcription-quantitative polymerase chain reaction and Western blot assays were performed to detect the expression of GTF3C2, ubiquitin specific peptidase 21 (USP21), mitogen-activated protein kinase 2 (MEK2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p-ERK1/2 in cells. A luciferase reporter assay was conducted to explore the regulatory effect of GTF3C2 on USP21 transcription. Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine, and colony formation assays were performed to assess HCC cell proliferation. Subcutaneous injection of HCC cells into nude mice was used to evaluate tumor growth in vivo.

GTF3C2 expression was upregulated in HCC tissues and was positively correlated with advanced tumor stages and high tumor grades. HCC patients with high GTF3C2 expression had significantly worse survival outcomes. Knockdown of GTF3C2 suppressed the proliferation of Hep3B and HCCLM3 cells, while overexpression of GTF3C2 facilitated the proliferation of SNU449 and Huh7 cells. GTF3C2 promoted USP21 expression by activating its transcription, which subsequently increased the levels of MEK2 and p-ERK1/2 in HCC cells. Overexpression of both USP21 and MEK2 counteracted the GTF3C2 knockdown-induced inactivation of the ERK1/2 pathway. Moreover, GTF3C2 promoted HCC cell proliferation in vitro and tumor growth in vivo by regulating the USP21/MEK2/ERK1/2 pathway.

Upregulation of GTF3C2 is frequently observed in HCC tissues and predicts poor prognosis. GTF3C2 promotes HCC cell proliferation via the USP21/MEK2/ERK1/2 pathway.

Acute coronary syndrome (ACS) in patients with SARS-CoV-2 infection is primarily driven by inflammation-induced myocardial injury through both direct and indirect mechanisms. Effective clinical management requires a dual approach: addressing cardiovascular lesions while also mitigating virus-induced local and systemic inflammation. This comprehensive approach is essential for improving the diagnosis and treatment of SARS-CoV-2-associated ACS. Emerging evidence highlights the potential of myocardial protective agents, including angiotensin-converting enzyme 2-modulating drugs and traditional Chinese medicine, which not only stabilize plaques and improve endothelial function but also confer cardioprotective effects. Furthermore, advancements in nanotechnology offer promising strategies for targeted therapy—particularly through angiotensin-converting enzyme 2 receptor modulation—by enhancing the precision and efficacy of herbal medicine delivery. This review explores the complex interplay between SARS-CoV-2 infection and ACS pathogenesis, and evaluates the therapeutic potential of pharmacological, herbal, and nanotechnology-based interventions in managing this multifaceted condition.

Shenqi Fuzheng (SQ) is a widely used Chinese medicine formula known for its immune-enhancing and Qi-supplementing properties. However, the blood-absorbed components of SQ and their pharmacokinetics remain underexplored. This study aimed to comprehensively analyze the chemical constituents of SQ and investigate their absorption and pharmacokinetic behavior in rat plasma.

Ultra-performance liquid chromatography-triple quadrupole time-of-flight mass spectrometry (hereinafter referred to as UPLC-Triple-TOF/MS) is employed to identify the chemical components in SQ extract and quantify the components absorbed into the blood after oral administration in rats. This method provides fragmentation patterns of compounds and key pharmacokinetic profiles of blood-absorbed compounds.

A total of 105 compounds are identified from the SQ extract, and 40 are detected in the blood following oral administration. Organic acids and amino acids are found at higher concentrations in the bloodstream. Compounds such as Astragalosides promptly enter the bloodstream within 5 m after administration, with levels declining after 15 m. Flavonoids are absorbed within 15–30 m, and the peak of alkaloids occurs approximately 1 h after administration.

This study provides new insights into the chemical composition and pharmacokinetics of SQ, highlighting the dynamic changes in the content of absorbed compounds in the blood. It further promotes the comprehensive characterization of traditional Chinese medicine formulations through UPLC-Triple-TOF/MS. Future research should focus on elucidating the pharmacological activities of the identified compounds and investigating their potential synergistic effects within the formulation.

circPVT1 has emerged as a key regulator in disease progression and clinical outcomes. However, its prognostic relevance and association with clinicopathological parameters in solid malignancies remain to be fully elucidated. To address this, we conducted a meta-analysis to elucidate the clinical significance of circPVT1 in solid tumors.

A comprehensive literature search was conducted across multiple databases, including PubMed, Web of Science, Embase, the Cochrane Library, and CNKI, with a cutoff date of December 31, 2024. Statistical analyses were conducted using STATA 12.0 to calculate pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs), assessing the impact of circPVT1 expression on overall survival (OS) and its association with clinicopathological characteristics.

This analysis included 27 clinical studies encompassing a total of 2,219 patients. Elevated circPVT1 expression was significantly associated with poorer OS in patients with solid tumors (HR = 1.68, 95% CI: 1.39–2.02, P < 0.001). This association was particularly notable in lung cancer (HR = 2.08, 95% CI: 1.51–2.88, P < 0.001) and osteosarcoma (HR = 1.65, 95% CI: 1.38–1.97, P < 0.001), with similar trends observed in hepatocellular carcinoma, colorectal cancer, and papillary thyroid carcinoma. Furthermore, the increased circPVT1 level was correlated with larger tumor size (OR = 1.36, 95% CI: 1.11–1.67, P = 0.004), lymph node metastasis (OR = 1.56, 95% CI: 1.22–2.00, P < 0.001), distant metastasis (OR = 1.80, 95% CI: 1.10–2.92, P = 0.017), and advanced tumor-node-metastasis stage (OR = 1.84, 95% CI: 1.50–2.25, P < 0.001).

Aberrant circPVT1 expression is associated with adverse OS and unfavorable clinicopathological features in solid tumors, underscoring its potential utility as a prognostic biomarker and indicator of tumor aggressiveness.

Philadelphia chromosome-positive (Ph+) B-lymphoblastic leukemia/lymphoma (B-ALL/LBL) is an aggressive hematologic malignancy driven by the BCR::ABL1 fusion. While many cases respond well to treatment, some patients exhibit persistent BCR::ABL1 expression after therapy, presenting significant diagnostic challenges.

We present the case of a seven-year-old girl diagnosed with Ph+ B-ALL. Despite low percentages or negative results for blasts post-treatment, molecular and cytogenetic studies persistently detected high levels of BCR::ABL1, suggesting a high disease burden at the genetic level. This discordance supported multilineage involvement and the potential for retrospective revision of the initial diagnosis to lymphoblast crisis of chronic myeloid leukemia (LBC-CML).

Classifying such cases as de novo Ph+ B-ALL with multilineage involvement or LBC-CML is challenging, as there is currently no consensus among experts. Further studies are necessary to clarify the distinction, given the different management strategies and treatment responses between these two conditions.

Gut dysbiosis has been reported in severe liver diseases. However, information on the impact of hepatitis E virus infection on the gut microbiota, and the association between enteric microbiota disturbances and acute hepatitis E (AHE), is limited, particularly in elderly patients with AHE (AHE-elderly). Our objective was to characterize the AHE-specific microbiome in elderly patients and evaluate its association with clinical outcomes.

Fecal samples and clinical data were collected from 58 AHE-elderly patients (46 self-healing cases, 12 non-self-healing cases) and 30 elderly patients with healthy controls (hereinafter referred to as HCs-elderly). Gut microbiota composition was analyzed using 16S rRNA gene sequencing. Bioinformatic analyses, including alpha diversity and STAMP, were performed. The predictive potential of Bacteroides fragilis was assessed using statistical analysis and receiver operating characteristic curves.

Alpha diversity indices showed no significant differences in microbial diversity between the AHE-elderly and HCs-elderly groups, nor between self-healing and non-self-healing groups among AHE-elderly patients. Nevertheless, a trend toward altered species richness was observed. In the AHE-elderly group, the relative abundance of Firmicutes, Lactobacillales, and Bacilli increased significantly. Meanwhile, compared with the self-healing group, Bacteroidetes were more abundant in the non-self-healing group. At the species level, Bacteroides fragilis was the most abundant in the non-self-healing group, significantly contributing to the divergence in gut microbiota between the two groups.

The relative abundance of Bacteroidetes significantly distinguished AHE-elderly patients from healthy controls and could more accurately predict recovery outcomes in elderly AHE patients. These findings suggest new strategies for preventing and managing AHE recurrence in the elderly patients.