As one of the commonest gynecological malignancies in the world, cervical cancer brings great threat for public health. Long non-coding RNAs (LncRNAs) have been proved to be closely related to the progression of various cancers, including cervical cancer. As a tumor promoter, lncRNA XIST has been reported in various malignant tumors. In this study, we aim to explore the specific mechanism and biological function of XIST in cervical cancer. At first, the expression levels of XIST were examined in both tissues and cell lines with qRT-PCR. XIST was extremely overexpressed in cervical cancer tissues and cell lines. Kaplan Meier method was then applied to analyze the correlation between XIST expression and overall survival of cervical cancer patients. Loss-of- function assays were designed and conducted to verify the oncogenic function of XIST on cervical cancer progression. Additionally, the results of mechanistic experiments indicated that XIST upregulated Fus through competitively binding with miR-200a. Finally, rescue assays were conducted to demonstrate the regulatory function of XIST-miR-200a-Fus axis in cervical cancer progression. Collectively, XIST served as a ceRNA in cervical cancer progression through modulating miR-200a/Fus axis.

Topical therapy with prostaglandin analogues is associated with CCT reduction. Latanoprost, travoprost, and bimatoprost have a similar effect on CCT.

The prognosis for patients with malignant glioma is very poor and thus the identification of new potential therapeutic targets is critically important. In this work, we report a previously unknown role for the homeobox transcription factor HOXC10 in regulating immunosuppressive gene expression in glioma cell lines and their proliferative and invasive capacities. Although HOXC10 expression is dysregulated in several types of tumors, its potential function in glioma was not known. We found that HOXC10 expression was upregulated in glioma compared with normal tissue, and that HOXC10 expression positively associated with high grading of glioma. In three independent datasets (REMBRANDT glioma, The Cancer Genome Atlas glioblastoma multiforme and GSE4412), HOXC10 upregulation was associated with short overall survival. In two glioma cell lines, HOXC10 knock-down inhibited cell proliferation, colony formation, migration and invasion, and promoted apoptosis. In addition, HOXC10 knock-down suppressed the expression of genes that are involved in tumor immunosuppression, including those for transforming growth factor-β 2, PD-L2, CCL2 and TDO2. A ChIP assay showed that HOXC10 directly bound to the PD-L2 and TDO2 promoter regions. In summary, our results suggest that HOXC10 upregulation in glioma promotes an aggressive phenotype and induces immunosuppressive gene expression, supporting further investigation of the potential of HOXC10 as a therapeutic target in glioma.