Abstract
BACKGROUND: Cervical cancer (CC) is a widely recognized malignant tumor that imposes a substantial economic burden on the global healthcare system. Currently, treatment options for patients with advanced metastatic and recurrent CC are suboptimal. Therefore, further in-depth research into the characteristics of CC occurrence and metastasis may provide additional reference indicators for patient diagnosis, treatment, and prognosis. This study aims to screen differential genes in CC via transcriptome sequencing and bioinformatics analysis, verify the role of microtubule-associated serine/threonine kinase 1 (MAST1) in CC, and explore its underlying molecular mechanisms, providing a basis for CC diagnosis and treatment. METHODS: In this study, we performed transcriptome sequencing on three cases of CC and adjacent normal tissues to understand the differences in gene expression profiles between cancerous and adjacent tissues. Bioinformatics methods were used to functionally enrich the differentially expressed genes, and these data were further analyzed to screen for the differential gene MAST1. The expression of the gene in tumor and adjacent normal tissues was detected through reverse transcription quantitative polymerase chain reaction (RT-qPCR), protein immunoblotting, and immunohistochemistry (IHC). Small interfering RNA (siRNA) was designed to construct a knockdown CC cell line, and the cell migration ability was verified through Transwell assays, and the expression of pathway-related proteins was detected by Western blotting. RESULTS: Transcriptome sequencing revealed that 40 genes were significantly upregulated, and 62 genes were significantly downregulated in CC tissues. Gene Ontology (GO) analysis indicated that the differentially expressed genes (DEGs) were predominantly related to the extracellular matrix, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that these genes were mainly enriched in pathways associated with glutamatergic synapses, axon guidance, and cancer. Combining The Cancer Genome Atlas (TCGA) sequencing results, five highly expressed genes (MISP, MAST1, MUC13, OLR1, and PAQR4) were selected. RT-qPCR, western blot, and IHC results confirmed that MAST1 expression was significantly higher in cancer tissues than in adjacent normal tissues. In vitro cell experiments showed that the knockdown of MAST1 in Hela cells reduced cell invasion ability and downregulated the p-AKT and p-P38 signaling pathways. CONCLUSIONS: This study contributes to a deeper understanding of the role of MAST1 in the invasion of CC, affecting the occurrence and development of malignant tumors in the cervix through the p-AKT and p-P38 classical signaling pathways, and can serve as a potential therapeutic target for patients with CC.