SERPINB7 as a prognostic biomarker in cervical cancer: Association with immune infiltration and facilitation of the malignant phenotype.

Purpose: The purpose of this study was to investigate the expression patterns, predictive significance, and roles in the immune microenvironment of Serpin Family-B Member 7 (SERPINB7) in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). Methods: The expression of SERPINB7 and its prognostic relevance were evaluated using RNA-seq data from The Cancer Genome Atlas. SERPINB7 regulation of CESC cell growth and metastasis was investigated using MTT, scratch, and Transwell assays. In vivo effects of SERPINB7 were examined in xenograft model mice and differentially expressed genes (DEGs) associated with SERPINB7 were identified to explore its functional role in oncogenesis. Associations between SERPINB7 levels, chemosensitivity, and immune infiltration were assessed, and mutations and methylation of SERPINB7 were evaluated using the cBioPortal and MethSurv databases, respectively. Results: SERPINB7 was up-regulated in CESC samples as well as in other tumors, and patients with higher SERPINB7A mRNA levels exhibited shorter overall survival. The area under the curve for the use of SERPINB7 in CESC diagnosis was above 0.9, and the gene was shown to regulate tumor cell proliferation and metastasis in vitro and in vivo. Overall, 398 DEGs enriched in key CESC progression-related signaling pathways were identified. SERPINB7 expression was additionally correlated with intratumoral immune infiltration and immune checkpoint activity. Patients expressing higher SERPINB7 levels exhibited distinct chemosensitivity profiles, and methylation of the SERPINB7 gene was linked to CESC patient prognostic outcomes. Conclusion: SERPINB7 was found to be a crucial regulator of CESC progression, prognosis, and the tumor immune microenvironment, highlighting its potential as a diagnostic and prognostic biomarker and target for CESC immunotherapy.

MicroRNA-374b reduces the proliferation and invasion of colon cancer cells by regulation of LRH-1/Wnt signaling.

Deregulation of microRNA (miRNA) has been suggested as a critical event in colon cancer development and progression. Recent studies have suggested that miR-374b is a novel cancer-related miRNA involved in several cancer types. Thus far, very little is known about the role of miR-374b in colon cancer; therefore, the goal of this study was to investigate the potential role of miR-374b in colon cancer. Here, we showed that miR-374b expression was significantly downregulated in colon cancer tissues and cell lines. Overexpression of miR-374b inhibited the proliferation and invasion of colon cancer cells, while miR-374b suppression promoted colon cancer cell proliferation and invasion. Liver receptor homolog-1 (LRH-1) was identified as a target of miR-374b in colon cancer cells. Both the mRNA and protein expression of LRH-1 were regulated by miR-374b. In addition, an inverse correlation between LRH-1 mRNA and miR-374b expression was evidenced in colon cancer specimens. Notably, overexpression of miR-374b also downregulated the Wnt signaling in colon cancer cells. Furthermore, restoration of LRH-1 expression significantly abolished the antitumor effect of miR-374b in colon cancer cells. These findings suggest that miR-374b inhibits colon cancer cell proliferation and invasion through downregulation of LRH-1 expression. Inhibiting LRH-1 by miR-374b may represent a novel therapeutic strategy for the treatment of colon cancer.