Growth arrest special 5 (GAS5) is a long non-coding RNA reported to function as an inhibitor in various tumors including cervical cancer. However, the molecular mechanism of GAS5 involved in cervical cancer progression remains far from being elucidated. The expression of GAS5, forkhead box protein O1 and phosphatase and tensin homolog was examined by quantitative reverse transcription polymerase chain reaction qRT-PCR. cell growth, invasion, and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay, transwell invasion assay, and flow cytometry analysis, respectively. The interaction between GAS5 and miR-196a or miR-205 was confirmed by luciferase reporter assay, RNA immunoprecipitation assay, and qRT-PCR. Xenograft tumor experiments were performed to validate the biological role of GAS5 and its molecular mechanism in cervical cancer in vivo. GAS5 expression was decreased in cervical cancer tissues and cells. GAS5 overexpression suppressed cervical cancer cell proliferation, invasion, and apoptosis. GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression. Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively. Exogenous expression of GAS5 hindered tumor growth in vivo by downregulating miR-196a and miR-205. Upregulation of GAS5 suppressed cell proliferation, invasion, and apoptosis of cervical cancer cells by downregulating miR-196a and miR-205, contributing to our understanding the pathogenesis of cervical cancer and development of long non-coding RNA–mediated clinical therapy against this disease.

This study aims to figure out the methylation of long non-coding RNA GAS5 promoter in cervical cancer and the mechanism of GAS5 on the progression of cervical cancer cells. The expression of GAS5 and methylation state of GAS5 in cervical cancer tissues and cells were determined. With the aim to to explore the ability of GAS5 in the proliferation, cell cycle progression, apoptosis, invasion, migration as well as the tumor growth, and metastasis in nude mice were determined. The expression of GAS5 was decreased and methylation state of GAS5 was elevated in cervical cancer.Overexpression of GAS5 inhibited proliferation, cell cycle progression, invasion, migration while inducing apoptosis of cervical cancer cells as well as suppressed tumor growth and metastasis in nude mice. Our study demonstrates that abnormal methylation of GAS5 contributes to poor expression of GAS5 in cervical cancer. In addition, upregulation of GAS5 inhibits the cervical cancer development. K E Y W O R D Scervical cancer, GAS5, growth, metastasis, promoter methylation

Cervical cancer remains a malignant type of tumor and is the fourth leading cause of cancer‐related death among females. MALAT1 has been identified as a tumor oncogene in various cancers. Our present study aimed to explore the biological role of MALAT1 in cervical cancer. We observed that MALAT1 was significantly upregulated in human cervical cancer cell lines compared with the ectocervical epithelial cells. MALAT1 was repressed by transfection with LV‐shMALAT1, whereas increased by LV‐MALAT1 in HeLa and Caski cells. Silencing of MALAT1 obviously reduced cervical cell viability, induced cell apoptosis, and repressed cell invasion capacity. Conversely, overexpression of MALAT1 exhibited an opposite phenomenon. Furthermore, miR‐429 was predicted as a direct target of MALAT1, and it was dramatically decreased in cervical cancer cells. It has been shown that miR‐429 plays a crucial role in cervical cancer progression. In our current study, the targeting correlation between MALAT1 and miR‐429 was confirmed by luciferase reporter assays and RIP experiments. Finally, in vivo animal models were established, and we indicated that MALAT1 inhibited cervical cancer progression via targeting miR‐429. These findings revealed that MALAT1 can sponge miR‐429 and regulate cervical cancer pathogenesis in vivo and in vitro. In conclusion, we indicated that the MALAT1/miR‐429 axis was involved in cervical cancer development.

Long non-coding RNAs (lncRNAs) are involved in the progression of several diseases. The interactions among lncRNAs, microRNA (miRNAs) or their targeting genes are reported to play crucial roles in the development of diseases. LINC00657 is observed to be upregulated in several cancers. However, the biological role of LINC00657 in neuropathic pain progress is unclear. Hence, in our study, we aimed to investigate the function of LINC00657 in neuropathic pain development. A chronic constriction injury (CCI) rat model was established, and we found that LINC00657 was greatly increased in CCI rats associated with a decrease of miR-136. Inhibition of LINC00657 suppressed neuropathic pain via alleviating mechanical and thermal hyperalgesia. In addition, miR-136 overexpression can also inhibit the neuropathic pain development. MiR-136 was predicted to serve as a miRNA target of LINC00657, and dual-luciferase reporter assay confirmed the correlation between LINC00657 and miR-136. Moreover, we observed that the decrease of LINC00657 was able to inhibit the neuroinflammation of CCI rats by targeting expression of cyclooxygenase-2, tumor necrosis factor-α and interleukin-1β while miR-136 inhibitors reversed this phenomenon. Next, by using bioinformatics analysis, ZEB1 was predicted as a direct target of miR-136, and miR-136 could negatively modulate ZEB1 expression. Besides these, ZEB1 was remarkably increased in the CCI rats. Knockdown of ZEB1 can inhibit neuropathic pain development, while miR-136 inhibitors can reverse it. In conclusion, it was implied that LINC00657 can induce the neuropathic pain development via regulating miR-136/ZEB1 axis.

Cervical cancer (CC) is the most common malignant tumor with poor clinical outcome among women. Identification of novel biomarkers could be beneficial for the clinical diagnosis and treatment of CC. This study aimed to identify prognostic biomarkers for the prediction of prognostic status of CC patients, and explore the effect of the corresponding methylated genes in the occurrence and development of CC. The methylation microarray data of CC was extracted from The Cancer Genome Atlas (TCGA) dataset. The methylation genes associated with the prognostic status were identified based on the information of the relapse-free survival (RFS) of the CC patients. The prognostic gene pairs were further identified. Then, the prognostic signature was identified by the forward search algorithm based on the C-index method. The results were validated by independent dataset. Finally, the functional analysis was performed on the methylation genes. A total of 276 methylation genes and 2508 gene pairs associated with the prognostic status of the CC were identified.A signature composed of eight methylation gene pairs was obtained to predict the prognostic status of cervical patients. A series of genes that played an important role in the occurrence and development of CC were obtained by the functional enrichment analysis. To summary, a prognostic signature consisting of eight methylation gene pairs was obtained. Of note, the CD28 and PTEN gene pair were found to play important roles in the occurrence and development of CC.

The induction of apoptosis by realgar is mediated through a cytochrome c-dependent pathway, which sequentially activates caspase-9 and caspase-3.

Solifenacin with or without local estrogen was effective and safe for overactive bladder treatment in postmenopausal women. The addition of local estrogen improved subjective feelings and QoL.

This study investigated the anti-HSV-2 effect of alumen through in vitro and in vivo experiments. Viable cell counting was employed to assess the toxicity of alumen on Vero cells. The inhibition rate of HSV-2 was defined as the cytopathic effect (CPE) of the cells infected with the virus. Alumen suppositories of different concentrations were vaginally applied to the guinea pigs which were then infected with HSV-2 via a vaginal route. The clinical symptoms were observed and the local virus titer calculated. The results showed that alumen had an in vitro anti-HSV-2 effect by means of antiviral duplication, direct killing of the virus, and antiviral adsorption. Alumen suppositories of different concentrations could reduce or completely inhibit HSV-2 infection in guinea pigs. It was concluded that alumen had an in vitro anti-HSV-2 effect through multiple approaches and it could suppress in vivo vaginal HSV-2 infection of guinea pig to some extent.