Dysregulation of the long noncoding RNA GAS5 in human cancer has been identified in recent studies. In this study, we confirmed a negative correlation between the GAS5 expression level and papillary thyroid carcinoma clinicopathologic characteristics, such as the tumor size, lymph node metastasis, the TNM stage and BRAFV600E mutation. The viability and metastasis of papillary thyroid carcinoma cells were detected by CCK-8 and transwell assays, respectively. The results showed that upregulation of GAS5 significantly inhibited papillary thyroid cancer cell growth, migration and invasion in vitro. RNA transcriptome sequencing was performed to explore the underlying targets of GAS5. Through qRT-PCR and Western blot analysis, we found that ectopic expression of GAS5 significantly increased IFI44 and STAT1 levels. Taken together, these findings suggest that GAS5 is a tumor suppressor in papillary thyroid carcinoma, and the action of GAS5 may be mediated through the IFNγ/STAT1 signaling pathway.

Background and aim Long non-coding RNAs (lncRNAs) are implicated as novel factors in tumorigenesis and tumor progression. Although thousands of lncRNAs have been discovered, only a small portion have been functionally determined in hepatocellular carcinoma (HCC). Here, we aimed to comprehensively analyze differentially expressed lncRNAs, evaluate their clinical significance, and explore the functional roles and underlying mechanism in HCC. Methods We identified hundreds of lncRNAs which were dysregulated in HCC tissues through performing integrative analyses using the RNA sequencing data and independent gene microarray data from Gene Expression Omnibus and the Cancer Genome Atlas. Results Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes. Further experimental validation revealed that down-regulation of lncRNA DUXAP8 inhibited HCC cells proliferation and colony formation ability. Mechanistically, DUXAP8 repressed tumor suppressor KLF2 transcription through interacting with histone-lysine N-methyltransferase enzyme enhancer of zeste homolog 2. Conclusion Taken together, our findings can provide a valuable resource of HCC-associated lncRNAs and new insights into the biological functions of lncRNAs in HCC development.

EZH2 is a core component of the polycomb repressive complex 2 (PRC2), which catalyzes trimethylation of histone H3 lysine 27 (H3K27me3) and promotes carcinogenesis by epigenetically silencing many tumor suppressor genes. Increased EZH2 expression is a marker of advanced and metastatic in many cancers, including lung, prostate and breast cancer, and it has been considered as a potential novel therapeutic target. However, the clinical significance and molecular mechanisms of EZH2 controlling gastric cancer cell proliferation and invasion are not well documented. In this study, immunohistochemical analysis was conducted to investigate the EZH2 expression in gastric cancer. We found that EZH2 levels were increased in gastric cancer tissues compared with adjacent normal tissues. Moreover, patients with high levels of EZH2 expression had a relatively poor prognosis. Furthermore, knockdown of EZH2 expression by siRNA could impair cell proliferation and invasion both in vitro and vivo. Finally, we found that EZH2 influences gastric cancer cells proliferation partly through regulating p21 expression. Our findings present that EZH2 over-expression can be identified as a poor prognostic biomarker in gastric cancer.

Recently, a growing number of evidence has revealed that long noncoding RNAs (lncRNAs) act as key regulators in various cellular biologic processes, and dysregulation of lncRNAs involves in tumorigenesis and cancer progression. However, the expression pattern, clinical relevance, and biologic function of most lncRNAs in human thyroid cancer remain unclear. To identify more thyroid-cancer-associated lncRNAs, we analyzed the expression profile of lncRNAs in thyroid cancer tissues and adjacent normal or non-tumor tissues using RNA sequencing data and gene microarray data from The Cancer Genome Atlas and Gene Expression Omnibus. Annotation and analyses of these data revealed that hundreds of lncRNAs are differentially expressed in thyroid cancer tissues when compared with normal tissues. By copy number variation analyses, we identified that some of those dysregulated lncRNAs genome locus are accompanied with the copy number amplification or deletion. Moreover, some lncRNAs expression levels are significantly associated with thyroid cancer patients overall or recurrence-free survival time, such as RUNDC3A-AS1, FOXD2-AS1, PAX8-AS1, and CRYM-AS1. Furthermore, we validated an lncRNA termed LINC00704 in thyroid cancer cells by performing loss of function assays. Downregulation of LINC00704 could significantly impair thyroid cancer cells proliferation, colony formation, inhibit cell-cycle progression and cell invasion, and induce cell apoptosis. Taken together, our findings reveal that lots of lncRNAs are dysregulated and may play critical roles in thyroid cancer, and this study could provide useful resource for identification and investigation of novel lncRNA candidates for thyroid cancer.