Construction of a novel cancer-associated fibroblast-related signature to predict clinical outcome and immune response in cervical cancer.

This study developed a prognostic signature for cervical cancer using transcriptome profiling and clinical data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and TISCH database, focusing on cancer-associated fibroblasts (CAFs). Through LASSO Cox regression and integrated bioinformatics analyses, we identified 144 differentially expressed genes (DEGs) related to CAFs, from which an 11-gene CAF-related signature (CAFRSig) was constructed. The CAFRSig effectively stratified patients into high- and low-risk categories, demonstrating significant prognostic capability in predicting overall survival. Gene ontology (GO) and gene set variation analysis (GSVA) linked the DEGs to crucial pathways in tumor malignancy, immune response, and fatty acid metabolism. The immune landscape analysis, utilizing the TIMER platform and CIBERSORT algorithm, revealed a positive correlation between immune cell effector functions and CAFRSig scores, highlighting the model's potential to identify patients likely to respond to immune checkpoint blockade (ICB) therapies. Furthermore, neuropilin 1 (NRP1), a key gene in the CAFRSig, was upregulated in cervical cancer tissues and associated with disease progression and differentiation. The downregulation of NRP1 curbed cell proliferation and influenced the epithelial-mesenchymal transition (EMT), implicating the PI3K/AKT pathway and modulating PD-L1 expression. This comprehensive analysis establishes a robust prognostic signature based on CAF-related genes, offering valuable insights for optimizing therapeutic strategies in cervical cancer management.

Knockdown of long non-coding RNA TUG1 suppresses nasopharyngeal carcinoma progression by inhibiting epithelial-mesenchymal transition (EMT) via the promotion of miR-384.

Nasopharyngeal carcinoma (NPC) is a cancer arising from the nasopharynx epithelium. Long non-coding RNAs (lnc RNA) play a critical role in various biological processes such as cell growth, embryonic development, and tumorigenesis. In the study, for the first time, we discovered that lnc RNA taurine upregulated gene 1 (TUG1) exhibited higher expression levels in NPC tissues and NPC cell lines than in normal nasopharyngeal epithelial tissues and normal nasopharyngeal cell line. In addition, patients with NPCs showing higher levels of TUG1 had worse overall survivals. Further, suppressing TUG1 expression markedly reduced the cell proliferation, migration and invasion; however, TUG1 over-expression significantly enhanced the proliferation, migration and invasion in NPC cells. TUG1 knockdown-inhibited epithelial-mesenchymal transition (EMT) was evidenced by the reduced expression of Vimentin, N-cadherin and transforming growth factor (TGF)-ß1, while the enhanced level of E-cadherin. The results of luciferase reporter analysis verified that miR-384 was a direct target of TUG1 in NPC, and was down-regulated in NPC tissues, exhibiting suppressive role in cell proliferation, migration and invasion. In vivo, TUG1 knockdown reduced tumor growth via the regulation of miR-384 by restraining EMT development. In conclusion, our findings suggested that there was a negative correlation between TUG1 and miR-384 in NPC patients. TUG1 might be an effective candidate for use in NPC diagnosis, prognosis and treatment.