Rujun Chen

Identification of m7G Methylation‐Related miRNA Signature Associated with Survival and Immune Microenvironment Regulation in Uterine Corpus Endometrial Carcinoma

Background. N7‐methylguanosine (m7G) has been implicated in the development of cancer. The role of m7G‐related miRNAs in the survival prediction of UCEC patients has not been investigated. Current research was the first to construct an m7G‐related miRNA model to accurately predict the survival of patients with uterine corpus endometrial carcinoma (UCEC) and to explore immune cell infiltration and immune activity in the tumor microenvironment. Methods. RNA‐seq data and clinical information of UCEC patients were derived from The Cancer Genome Atlas (TCGA) database. Using the TargetScan online database, we predicted miRNAs linked to the m7G‐related genes and identified miRNAs which were significantly associated with the survival in UCEC patients and constructed a risk scoring model. The TCGA‐UCEC cases were scored according to the risk model, and the high‐ and low‐risk groups were divided by the median risk value. Gene enrichment analysis and immune cell infiltration and immune function analysis were performed using “clusterProfiler” and “GSVA” packages in R. Results. The survival prediction model consisted of 9 miRNAs, namely, hsa‐miR‐1301, hsa‐miR‐940, hsa‐miR‐592, hsa‐miR‐3170, hsa‐miR‐876, hsa‐miR‐215, hsa‐miR‐934, hsa‐miR‐3920, and hsa‐miR‐216b. Survival of UCEC patients in the high‐risk group was worse than that in the low‐risk group (p < 0.001). The receiver operating characteristic (ROC) curve showed that the model had good predictive performance, and the area under the curve was 0.800, 0.690, and 0.705 for 1‐, 3‐, and 5‐year survival predictions, respectively. There were differences in the degree of immune cell infiltration and immune activity between the low‐risk and high‐risk groups. The expression levels of the identified differentially expressed genes correlated with the susceptibility to multiple anticancer drugs. Conclusions. The survival prediction model constructed based on 9 m7G‐related miRNAs had good predictive performance.

Elevated INHBA Promotes Tumor Progression of Cervical Cancer

Objectives: This study aimed to explore the role of inhibin subunit beta A (INHBA) in the progression of cervical cancer (CCa) and investigate its potential as a therapeutic target. Specifically, the objectives were to assess the expression levels of INHBA in CCa, examine its correlation with patient survival, and elucidate its impact on CCa cell proliferation, cell cycle regulation, migration, invasion, and in vivo tumor growth and metastasis. Methods: To achieve the objectives, we conducted a comprehensive set of experimental methods. INHBA expression in CCa was analyzed, and its association with patient survival was assessed using clinical data. In vitro experiments involved the investigation of INHBA's effects on CCa cell proliferation, cell cycle dynamics, migration, and invasion through the epithelial–mesenchymal transition (EMT) process. Additionally, in vivo experiments were performed to evaluate the influence of INHBA on CCa growth and lung metastasis. Results: The results of this study revealed upregulated expression of INHBA in CCa, with a significant association between high INHBA expression and poor patient survival. Functionally, INHBA was found to promote the proliferation of CCa cells, regulate the cell cycle, and enhance migration and invasion through the EMT process in vitro. Moreover, in vivo experiments demonstrated that INHBA facilitated the growth and lung metastasis of CCa. Conclusion: In conclusion, our findings suggest that INHBA plays a crucial role in the progression of cervical cancer. The upregulation of INHBA is associated with poor patient survival, and its involvement in promoting key aspects of cancer progression makes it a potential therapeutic target for CCa treatment. These results provide valuable insights into the molecular mechanisms underlying CCa and offer a foundation for further exploration of targeted therapeutic interventions.