Cervical cancer (CC) is a common malignant tumor among women worldwide, remaining the fourth most frequent cause of cancer death in women. Currently, microRNA (miRNA) is a prevalent topic in tumor-related research. The present study focused on the mechanisms of miR-100 in CC progression. qRT-PCR analysis revealed that the miR-100 expression was notably decreased in CC tissues. In addition, miR-100 downregulation was confirmed to be significantly related to the malignant clinicopathologic features of CC patients. Furthermore, miR-100 overexpression was also verified to significantly repress CC cell proliferation, migration and invasion abilities through modulating the AKT/mTOR signaling pathway and epithelial-to-mesenchymal transition. Bioinformatics analysis and luciferase reporter assay identified that special AT-rich sequence-binding protein 1 was a functional target for miR-100 in CC cells. Moreover, miR-100 overexpression was found to markedly repress the CC tumor growth in vivo. In conclusion, the above results revealed that miR-100 functioned as a cancer suppressor in CC progression and may provide insights into the novel therapeutic target for CC treatment.
Keywords: AKT/mTOR; SATB1; cervical cancer; epithelial-to-mesenchymal transition; miRNA-100.
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