Objective To investigate the expression and clinical significance of cytokeratin 7 (CK7) and aspartic peptidase A (NapsinA) in pleural effusion of lung adenocarcinoma (LUAD). Methods A total of 86 patients with LUAD and pleural effusion who were admitted to Kaifeng Central Hospital from February 2023 to February 2025 were selected. Meanwhile, 40 samples of benign pleural effusion (pleural effusion caused by tuberculous pleurisy, heart failure, etc.) were collected. The expression of CK7 and NapsinA in pleural effusion cells was detected by immunohistochemical method. The relationship between CK7, NapsinA and clinicopathological features of patients with LUAD and pleural effusion was analyzed. Results The positive expression rates and scores of CK7 and NapsinA in pleural effusion of patients with LUAD were higher than those in benign pleural effusion (P<0.05). ROC curve showed that CK7 and NapsinA had vertain value in differential diagnosis of LUAD and other diseases (P<0.05). Among 86 patients with LUAD, CK7 expression and NapsinA expression were high in 37 cases (43.02%) and 41 cases (47.67%), respectively. No statistically significant differences were found in the high expression rates of CK7 and NapsinA when compared across patient gender, age, smoking status, T stage, and presence of extrathoracic metastasis (P>0.05). The high expression rate of CK7 in patients with epidermal growth factor receptor (EGFR) gene mutation was significantly higher than that in those without (P<0.05), but there was no statistically significant difference in the high expression rate of NapsinA between the two groups (P>0.05). Conclusion The positive expression rates of CK7 and NapsinA in pleural effusion of LUAD are high. Both have certain value in diagnosing LUAD and can serve as biological markers to distinguish benign and malignant pleural effusion. There is also a correlation between CK7 expression and EGFR gene mutation.

Objective To analyze the changes in serum levels of periostin (POSTN), pentraxin-3 (PTX3), and soluble fms-like tyrosine kinase receptor 1 (sFlt-1) in children with Henoch-Schönlein purpura nephritis (HSPN) and their clinical significance. Methods A total of 77 pediatric patients diagnosed with HSPN and admitted to the Jinshui District General Hospital, Zhengzhou City, from October 2021 to February 2024 were enrolled as the study group, while another 77 healthy individuals undergoing physical examinations during the same period served as the control group. At admission, serum levels of POSTN, PTX3, and sFlt-1, along with urinary microalbumin, creatinine, and urea nitrogen, were compared between the two groups to analyze their correlations. Additionally, the serum marker levels were compared among patients stratified by different pathological grades and clinical outcomes at admission, and their predictive value for clinical outcomes was investigated. Results The levels of serum POSTN, PTX3, sFlt-1, along with urinary microalbumin, creatinine, and urea nitrogen at admission in the study group were significantly higher than those in the control group (P<0.05). The serum levels of POSTN, PTX3, and sFlt-1 at admission in patients were positively correlated with renal function, urinary microalbumin, creatinine, and blood urea nitrogen (P<0.05). The serum levels of POSTN, PTX3 and sFlt-1 at admission in children with nephritis grade I-III were significantly lower than those in children with nephritis grade Ⅳ-Ⅵ (P<0.05); compared with the children with treatment failure, the serum levels of POSTN, PTX3 and sFlt-1 at admission in the effective children were significantly lower (P<0.05); the AUCs for predicting treatment failure based on serum POSTN, PTX3, sFlt-1 levels individually and jointly at admission were 0.837, 0.828, 0.832, and 0.935, respectively. Conclusion Serum POSTN, PTX3, and sFlt-1 play a role in the onset and progression of HSPN and are correlated with the renal pathological conditions in children with HSPN. These markers can effectively indicate the clinical therapeutic efficacy in children and hold significant value in predicting treatment outcomes.

Objective To investigate the correlation between the levels of serum tripartite domain protein 27 (TRIM27), tumor necrosis factor-like weak apoptosis-inducing factor (TWEAK), and Lin-28 homolog B (Lin28B) and the pathological characteristics and clinical prognosis of endometrial cancer (EC) patients. Methods A total of 115 EC patients admitted to the Second People's Hospital of Jiaozuo from June 2021 to June 2024 were selected as the study group, and 115 healthy physical examination subjects in the same period as the control group. The levels of serum TRIM27, TWEAK and Lin28B mRNA were compared between the two groups. The levels of TRIM27, TWEAK and Lin28B mRNA in patients with different pathological characteristics and prognosis in the study group were compared. The correlation between serum TRIM27, TWEAK and Lin28B mRNA levels and pathological characteristics and prognosis was analyzed. The receiver operating characteristic (ROC) curve and area under the curve (AUC) were used to analyze the diagnostic value of serum TRIM27, TWEAK and Lin28B mRNA for EC. Results The levels of serum TRIM27, TWEAK and Lin28B mRNA in the study group were higher than those in the control group (P<0.05). There were statistically significant differences in serum TRIM27, TWEAK and Lin28B mRNA levels in patients with different FIGO stages, tumor diameters and lymph node metastasis in the study group (P<0.05). The levels of serum TRIM27, TWEAK and Lin28B mRNA were positively correlated with FIGO stage, tumor diameter and lymph node metastasis (P<0.05). The AUC of serum TRIM27, TWEAK and Lin28B mRNA alone and combined diagnosis of EC was 0.712, 0.735, 0.685 and 0.857, respectively, and the combined AUC was the highest. The levels of serum TRIM27, TWEAK and Lin28B mRNA in patients with good prognosis were lower than those in the control group (P<0.05). Serum TRIM27, TWEAK and Lin28B mRNA levels were positively correlated with prognosis (P<0.05). Conclusion The high expression of TRIM27, TWEAK, and Lin28B mRNA in the serum of EC patients is closely related to their pathological characteristics and prognosis. TRIM27, TWEAK, and Lin28B can serve as auxiliary markers for diagnosing EC.

Objective To explore the mechanism of cordycepin (Cor) in the treatment of non-small cell lung cancer ( NSCLC ) by network pharmacology, molecular docking and in vitro experiments. Methods Multiple databases were used to search the targets of Cor and the therapeutic targets of NSCLC, and the common targets were screened out. STRING database and Cytostape were used to analyze and visualize the protein-protein interaction networks (PPI). GO and KEGG enrichment analysis was performed using the DAVID database, and the results were visualized using the online tool “Weishengxin”. AutoDock Vina was used to verify the molecular docking of Cor with the core target, and the binding energy was calculated. PyMol was used to visualize the results. MTT assay was used to detect the effect of Cor on the proliferation of NSCLC A549 cells. Western blot was used to detect the effect of Cor on the expression of core target proteins PARP1, P53 and AKT1. Results A total of 215 targets of Cor and 1238 therapeutic targets of NSCLC were screened, and 122 common targets were obtained. After PPI analysis, the core targets PARP1, P53 and AKT1 were selected according to Degree value for verification. The results of GO and KEGG enrichment analysis showed that biological process (BP) mainly involved apoptosis process, positive and negative regulation of gene expression, cellular component ( CC ) mainly involved cytoplasm and nucleus, molecular function (MF) mainly involved protein binding and enzyme binding, and signaling pathways mainly involved cancer, PI3K / AKT and other signaling pathways. Molecular docking showed that the three targets of PARP1, P53 and AKT1 were highly correlated with the treatment of NSCLC. In vitro experiments showed that Cor could inhibit the proliferation of human NSCLC A549 cells, significantly up-regulate the expression of P53 and PARP1 and down-regulate the expression of AKT1. Conclusion Cor inhibits the proliferation of human NSCLC A549 cells, and the mechanism may be related to the regulation of PARP1, P53 and AKT1 expression.

Objective To investigate the mechanistic role of LncRNA MITA1 in the progression of hepatocellular carcinoma (HCC). Methods qRT-PCR was employed to assess the expression levels of MITA1 mRNA in HCC tissues and cells. The pcDNA3.1 recombinant plasmid vector was utilized to overexpress MITA1. After treatment, SMMC7721 cells were categorized into three groups, the normal group, the OE-MITA1-NC (negative control) group, and the OE-MITA1 (overexpression) group. Cell proliferation was evaluated using a colony formation assay, while cell invasion was assessed via the Transwell assay. Cell viability was determined using the Cell Counting Kit-8 (CCK-8) assay. Protein expression levels of Vimentin, MMP-2, and N-Cadherin were measured by western blotting. Additionally, the dual-luciferase reporter assay was conducted to verify the targeting relationship between MITA1 and miR-30b-3p. Results Compared with adjacent normal liver tissues, HCC tissues and cells exhibited significantly higher expression levels of MITA1 mRNA and lower expression levels of miR-30b-3p mRNA (P<0.05). Under MITA1 overexpression conditions, the OE-MITA1 group demonstrated elevated MITA1 mRNA expression levels (P<0.05). Compared with the normal and OE-MITA1-NC groups, the OE-MITA1 group exhibited increased cell proliferation, invasion capacity, and enhanced cell viability (P<0.05). Furthermore, protein expression levels of Vimentin, MMP-2, and N-Cadherin were significantly higher in the OE-MITA1 group compared with the other two groups (P<0.05). The dual-luciferase reporter assay confirmed a targeting relationship between MITA1 and miR-30b-3p, with MITA1 expression negatively regulating miR-30b-3p expression. Conclusion LncRNA MITA1 can promotes the proliferation, invasion and cell activity of liver cancer by binding miR-30b-3p, MITA1 may serve as a potential therapeutic target for the diagnosis and treatment of HCC.