Inflammasome mediates the maturation of interleukin-1β (IL-1β) and IL-18, triggers the pyroptosis and associates with multiple autoimmune diseases. In light of this, we hope to investigate the regulatory role of miRNA-214 in the inflammasome of cervical cancer. With the samples collected from 50 cervical cancer patients and 50 age-matched healthy subjects, real-time PCR and Western blotting were employed to detect the mRNA and/or protein expression profiles of the NOD-like receptor protein family, including NLRP1, NLRP3, NLRC4, Caspase-1, IL-1β, IL-18 and miR-214. Corresponding plasmids were used to transfect the Hela, HCC94, Siha or HUCEL normal cell lines to upregulate or downregulate the expression of targeted genes and to construct the cervical cancer models on rats. In addition, RT-PCR and Western blot were also considered to detect the expression of miR-214 and pyroptosis-related genes, while the pyroptosis of cells was evaluated by using the caspase-1 activity detection kit. Downregulation of miR-214 was found in the cervical cancer patients and the cervical cancer cell lines (** P <0.01), while overexpression of miR-214 could induce the pyroptosis of cervical cancer cell by targeting NLRP3. In cervical cancer patients, miR-214 and NLRP3 are downregulated, while upregulation of miR-214, by enhancing the expression of NLRP3, can advance the pyroptosis of cervical cancer cells. In addition, we, for the first time, clarify the correlation of cervical cancer with the miR-214 and NLRP3.

Purpose MicroRNA-936 (miR-936) was previously reported to be dysregulated and involved in the development of non-small cell lung cancer and glioma. However, the functional roles of miR-936 in epithelial ovarian cancer (EOC) remain unclear. In this study, we aimed to evaluate miR-936 expression in EOC and investigate its regulatory role in EOC cell behavior. Methods The expression of miR-936 in EOC was measured by RT-qPCR. Cell proliferation, apoptosis, migration, and invasion in vitro, as well as tumor growth in vivo, were determined by CCK-8, flow cytometry, migration and invasion assays, and xenograft models in nude mice, respectively. Bioinformatics analysis, luciferase reporter assays, RT-qPCR, and Western blot analysis were performed to investigate the relationship between miR-936 and fibroblast growth factor 2 (FGF2). Results miR-936 expression was significantly downregulated in EOC tissues and cell lines. Low miR-936 expression was found to be correlated with the tumor size, FIGO stage, and lymphatic metastasis in EOC patients. Functional experiments indicated that ectopic miR-936 expression suppressed EOC cell proliferation, migration, and invasion; promoted cell apoptosis; and decreased tumor growth in vivo. In addition, the FGF2 gene was verified to be a direct target of miR-936 in EOC cells. FGF2 expression levels were upregulated in EOC tissues and were inversely correlated with miR-936 expression. Furthermore, effects of FGF2 silencing were similar to those of miR-936 overexpression in EOC cells. Recovered FGF2 expression rescued the miR-936-induced inhibitory effects in EOC cells. Notably, miR-936 was able to deactivate the PI3K/Akt signaling pathway in EOC cells by regulating FGF2 both in vitro and in vivo. Conclusion Altogether, our findings provided initial evidence that miR-936 inhibits the aggressiveness of EOC cells in vitro and in vivo, at least partially, by targeting FGF2-mediated suppression of the PI3K/Akt pathway. Therefore, the miR-936/FGF2/PI3K/Akt pathway is a promising therapeutic target for the treatment of EOC patients.

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We investigated the role of leucine-rich repeats and immunoglobulin-like domains (LRIG)-1 in ovarian cancer cell line and VP16 drug-resistant cell line to explore the possible mechanism of action. Human ovarian cancer cell line SKOV3 and the VP16 drug-resistant cell line SKOV3/VP16 were used to investigate whether LRIG1 affects the sensitivity of SKOV3 to drugs. RT-qPCR was used to detect the difference in LRIG1 expression between drug-resistant and wild-type cell lines. siRNA LRIG1 was designed and transfected to silence LRIG1 to investigate the mechanism by which LRIG1 affects the sensitivity of SKOV3 to drugs. Wild-type cells were transfected with SKOV3. The cells were divided into 3 groups (VP16, NC + VP16 and siRNA LRIG1 + VP16 treatment group). VP16 (IC50 value) was added 24 h after transfection. The CCK-8 method was used to detect the proliferation of each group at multiple time points (0, 24, 48 and 72 h). A colony-forming assay was used to detect cell proliferation and flow cytometry was used to detect cell apoptosis. The expression of LRIG1 was lower in the drug resistant cell line than that of the wild-type cell line. The expression of LRIG1 significantly decreased with the increase of VP16 concentration (P<0.05). The apoptotic rate was decreased but there was an increase on cell clones in the siLRIG1 + VP16-treated group as compared to VP16- and NC+ VP16-treated groups (P<0.05). The LRIG1 gene affects the sensitivity of SKOV3 cells to drug in a dose-related manner, indicating that the reduced expression of LRIG1 can inhibit cell apoptosis.