This study aimed at elucidating the molecular mechanism of miR-381-3p in cervical cancer progression, which may provide a novel therapeutic target for patients with cervical cancer. The expression of miR-381-3p was confirmed by quantitative reverse transcription polymerase chain reaction. Microarray analysis was conducted to screen out differentially expressed genes, and the target gene of microRNA (miRNA) was predicted on TargetScan. Dual-luciferase reporter assay then verified the targeting relationship between miR-381-3p and FGF7. The protein expression of FGF7 was examined via Western blot assay. Colony formation assay was used to detect the cell proliferation, while flow cytometry was used to analyze cell cycle and apoptosis. The influence of miR-381-3p and FGF7 on cell migration and invasion was confirmed by transwell migration/invasion assay. Finally, we demonstrated that miR-381-3p was lowly expressed, while FGF7 was highly expressed in cervical cancer cells. There was a direct target relationship and a negative correlation between miR-381-3p and FGF7. miR-381-3p could downregulate FGF7 expression, inhibiting cell proliferation and metastasis, and inducing cell cycle arrest and apoptosis in cervical cancer.

Cervical cancer is a common tumor of the reproductive system; however, to the best of the authors' knowledge, the regulation and underlying mechanism of p53 apoptosis-stimulating protein 2 (ASPP2) in cervical cancer has yet to be elucidated. Therefore, the present study aimed to explore the role of ASPP2 in cervical cancer. Tumor tissues were collected for the detection of ASPP2 expression. Experiments wherein ASPP2 was overexpressed were designed to upregulate the expression of ASPP2. The levels of autophagy were subsequently assessed by examining LC3B level via immunofluorescence. Cell Counting Kit-8 assay was then performed to estimate the level of cell proliferation. The cell proliferation level was also measured by EdU staining, and TUNEL assay was used to detect the level of apoptosis. The expression levels of ASPP2, Beclin1 and associated proteins were detected using reverse transcription-quantitative PCR and western blotting analyses. ASPP2 was observed to be markedly reduced in patients with cervical cancer and in cervical cancer cell lines. Overexpression of ASPP2 was found to suppress the expression of Beclin1, and autophagy was also inhibited in cervical cancer cells. Overexpression of ASPP2 also inhibited cell proliferation and promoted apoptosis of cervical cancer cells via the inhibition of autophagy. Additionally, overexpression of ASPP2 was shown to enhance the TNF-related apoptosis-inducing ligand-induced apoptosis of cervical cancer cells via inhibiting autophagy. Taken together, the results of the present study have shown that ASPP2 exerted antitumor effect in cervical cancer by inhibiting cell proliferation and promoting apoptosis partly through inhibiting autophagy. These findings may be useful for the provision of potential targets for cervical cancer therapy.