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<b><i>Objective:</i></b> The aim of this study was to investigate the effects of trichostatin A (TSA) on cervical cancer and the related mechanisms. <b><i>Methods:</i></b> The HeLa and Caski cervical cancer cell lines were treated with different concentrations of TSA. Cell viability was measured by MTT assays. Cell apoptosis was analysed using flow cytometry. Expression of transient receptor potential cation channel, subfamily V, member 6 (TRPV6), protein arginine methyltransferase 5 (PRMT5), and stanniocalcin 1 (STC1) was determined by qRT-PCR and Western blotting. Protein levels of LC3 II/I, beclin1, p62, JNK, and p-JNK were detected by Western blotting. <b><i>Results:</i></b> Treatment with TSA significantly decreased HeLa and Caski cell viability and enhanced the apoptosis rate in a dose-dependent manner. TSA markedly elevated beclin1 protein levels and the LC3 II/I ratio and significantly reduced p62 levels in a dose-dependent manner. In addition, TSA (1 μM) significantly suppressed PRMT5 and TRPV6 levels and enhanced STC1 and p-JNK levels. The lysosomal inhibitor bafilomycin-A1 synergistically enhanced the TSA-mediated increase in autophagic flux. Either the overexpression of TRPV6 or the inhibition of JNK signalling markedly enhanced cell viability, inhibited apoptosis, and autophagy and reduced p-JNK levels in TSA-treated cells. The inhibition of STC1 significantly increased TRPV6 protein levels and reduced p-JNK levels. Overexpression of PRMT5 dramatically decreased STC1 and p-JNK protein levels and increased TRPV6 levels. <b><i>Conclusion:</i></b> TSA suppresses cervical cancer cell proliferation and induces apoptosis and autophagy through regulation of the PRMT5/STC1/TRPV6/JNK axis.

Nasopharyngeal carcinoma (NPC) is a heterogeneous carcinoma whose underlying molecular mechanisms involved in tumor initiation, progression, and migration are largely unclear. The aim of the present study was to identify key biomarkers and small-molecule drugs for screening, diagnosing, and treating NPC via gene expression profile analysis. Raw microarray data was used to identify 430 differentially expressed genes (DEGs) in the Gene Expression Omnibus (GEO) database. The key modules associated with histological grade and tumor stage were identified using weighted gene co-expression network analysis. qRT-PCR was used to verify the differential expression of hub genes. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and the connectivity map database were used to identify potential mechanisms and screen smallmolecule drugs targeting hub genes. Functional enrichment analysis showed that genes in the green module were enriched in the regulation of cell cycle, p53 signaling pathway, and cell part morphogenesis. Four DEG-related hub genes (CRIP1, KITLG, MARK1, and PGAP1) in the green module, which were considered potential diagnostic biomarkers, were taken as the final hub genes. The expression levels of these four hub genes were verified via qRT-PCR, and the results were consistent with findings from the GEO analysis. Screening was also conducted to identify small-molecule drugs with potential therapeutic effects against NPC. In conclusion, four potential prognostic biomarkers and several candidate small-molecule drugs, which may provide new insights for NPC therapy, were identified.

Background Nasopharyngeal carcinoma (NPC) is a heterogeneous carcinoma that the underlying molecular mechanisms involved in the tumor initiation, progression, and migration are largely unclear. The purpose of the present study was to identify key biomarkers and small-molecule drugs for NPC screening, diagnosis, and therapy via gene expression profile analysis. Methods Raw microarray data of NPC were retrieved from the Gene Expression Omnibus (GEO) database and analyzed to screen out the potential differentially expressed genes (DEGs). The key modules associated with histology grade and tumor stage was identified by using weighted correlation network analysis (WGCNA). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of genes in the key module were performed to identify potential mechanisms. Candidate hub genes were obtained, which based on the criteria of module membership (MM) and high connectivity. Then we used receiver operating characteristic (ROC) curve to evaluate the diagnostic value of hub genes. The Connectivity map database was further used to screen out small-molecule drugs of hub genes. Results A total of 430 DEGs were identified based on two GEO datasets. The green gene module was considered as key module for the tumor stage of NPC via WGCNA analysis. The results of functional enrichment analysis revealed that genes in the green module were enriched in regulation of cell cycle, p53 signaling pathway, cell part morphogenesis. Furthermore, four DEGs-related hub genes in the green module were considered as the final hub genes. Then ROC revealed that the final four hub genes presented with high areas under the curve, suggesting these hub genes may be diagnostic biomarkers for NPC. Meanwhile, we screened out several small-molecule drugs that have provided potentially therapeutic goals for NPC. Conclusions Our research identified four potential prognostic biomarkers and several candidate small-molecule drugs for NPC, which may contribute to the new insights for NPC therapy.