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Studies have proved the role of GAS5 in the development of different cancers. This study was undertaken to investigate the role and explore therapeutic implications of GAS5 in human cervical cancer. The results showed that GAS5 was significantly (p < 0.05) downregulated in human cervical cancer tissues. The results also showed that cervical cancer progresses with the suppression of GAS5 expression levels. Additionally, the expression of GAS5 was also significantly (p < 0.05) downregulated in human cervical cancer cell lines. Nonetheless, overexpression of GAS5 caused a remarkable decrease in the proliferation of C33A and HeLa cervical cancer cells. The decrease in the proliferation rate was attributed to the induction of apoptosis of C33A and HeLa cells which was accompanied with upregulation of Bax and suppression of Bcl-2. Additionally, GAS5 overexpression also promoted the arrest of C33A and HeLa cells at the G2/M check point of cell cycle via suppression of cyclin B1 and CDK1 expression. The transwell assays showed that GAS5 overexpression significantly (p < 0.05) inhibited the migration and invasion of the C33A and HeLa cervical cancer cells. The bioinformatics analysis as well as the dual luciferase assay showed GAS5 acts as a target of miR-135a. Interestingly, the expression of miR-135a was upregulated in the human cervical cancer cells and its suppression exerted growth inhibitory effects on the C33A and HeLa cells. However, silencing of GAS5 could nullify the effects of miR-135a suppression on the proliferation of C33A and HeLa cells. Taken together, the results of this study point towards the therapeutic implications of GAS5 in the treatment of cervical cancer. [ABSTRACT FROM AUTHOR]

Purpose: To explore miRNA-875-5p and epidermal growth factor receptor (EGFR) activities in tissues or cells from cervical cancer, and their underlying molecular mechanisms. Methods: Tissues were obtained from cervical cancer patients and their miR-875-5p expression was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Caski or HeLa cells were transfected with miR-875-5p mimics or miR-875-5p inhibitor to assess the effect of miR-875- 5p expression on cell viability, cell cycle, migration, and invasion using Cell Counting Kit-8 (CCK-8), flow cytometry, wound healing, and Transwell assays. Potential target genes of miR-875-5p were predicted and verified using a dual luciferase reporter assay. In addition, EGFR expression was evaluated by western blot. Results: MicroRNA-875-5p was expressed at low levels in cervical cancer tissues and was related to FIGO stage, lymph node metastasis, pathological grade, vascular involvement, and deep stromal invasion in patients with cervical cancer. MicroRNA-875-5p overexpression inhibited cell viability, migration, and invasion, and caused G0/G1 phase block of Caski and HeLa cells. Moreover, EGFR was the target gene of miR-875-5p and was negatively regulated by miR-875-5p. Reductions in cell viability, migration, invasion, and the number of G0/G1-phase cells were inhibited by EGFR overexpression. Conclusion: MiR-875-5p suppresses cervical cancer cell growth and metastasis by negatively regulating EGFR. Therefore, miR-875-5p can potentially be exploited for the management of cervical cancer. [ABSTRACT FROM AUTHOR]