Small nucleolar RNA host gene 15 (SNHG15) has been suggested to be overexpressed, and function as an oncogenic long noncoding RNA (lncRNA) in various types of human malignancies. However, the expression status and function of SNHG15 were still unknown in thyroid cancer. In our study, we assessed the expression status and clinical value in thyroid cancer samples, and explored the effect of SNHG15 on thyroid cancer cell proliferation, migration, and invasion. In results, SNHG15 expression was downregulated in thyroid cancer tissues and cells, and correlated with age, pathology classification, clinical stage, tumor size, distant metastasis, and disease‐free survival. The in vitro studies suggested SNHG15 overexpression suppressed cell proliferation, migration, and invasion in thyroid cancer. In summary, SNHG15 serves as tumor suppressive role in thyroid cancer.

Background Pancreatic ductal adenocarcinoma (PDAC), a subtype of pancreatic cancer, is a malignant tumor with unfavorable prognosis. Despite accumulating researches have made efforts on finding novel therapeutic methods for this disease, the underlying mechanism of long non-coding RNAs (lncRNAs) remains elusive. OIP5 antisense RNA 1 (OIP5-AS1) has been reported to play important role in the occurrence and development of multiple human cancers. This study was aimed at unveiling the regulatory role of OIP5-AS1 in PDAC. Methods RT-qPCR analysis revealed the OIP5-AS1 expression in PDAC tissues and adjacent normal ones. Kaplan–Meier method was applied to analyze the overall survival of patients with high or low level of OIP5-AS1. Gain- or loss-of function assays were performed to assess the effects of OIP5-AS1 knockdown on cell functions, including proliferation, migration and EMT process. Mechanism experiments, such as luciferase reporter and RNA pull-down assays proved the interaction between OIP5-AS1 and miR-429 as well as that between miR-429 and FOXD1. Results OIP5-AS1 was up-regulated in PDAC tissues and cell lines, and high level of OIP5-AS1 indicated poor prognosis in PDAC patients. OIP5-AS1 knockdown hindered cell proliferation, migration and epithelial-mesenchymal transition (EMT) process, while overexpression of OIP5-AS1 caused the opposite results. OIP5-AS1 activated ERK pathway through up-regulating forkhead box D1 (FOXD1) expression by sponging miR-429. Furthermore, OIP5-AS1 facilitated cell growth in vivo. Conclusion OIP5-AS1 exerted oncogenic function in PDAC cells through targeting miR-429/FOXD1/ERK pathway.

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Pancreatic cancer (PC), one of the most aggressive and lethal human malignancies, is associated with a deplorable prognosis despite progressive therapeutic strategies.Emerging evidence manifests that miR-28-5p is involved in several cancers, and its descending expression is associated with poor prognosis. Nevertheless, the function of miR-28-5p in PC remains unclear. Thus, the underlying regulatory mechanism of miR-28-5p in PC is urgent to be clarified. In the present study, we first recognized miR-28-5p was downregulated in PC, and miR-28-5p overexpression inhibited cell proliferation and migration in PC. Then miR-28-5p was verified to act as a molecular sponge of LOXL1-AS1. Therefore, the function of LOXL1-AS1 was further explored in PC, presenting that LOXL1-AS1 suppression inhibited cell proliferation and migration. What is more, SEMA7A was found to be a target gene for miR-28-5p and was upregulated in PC. In addition, LOXL1-AS1 could positively regulate SEMA7A expression while miR-28-5p could negatively regulate SEMA7A expression. According to rescue experiments, SEMA7A overexpression partially neutralized LOXL1-AS1 silence-mediated inhibitory function on progression in PC. Taken together, all the data demonstrated that LOXL1-AS1/miR-28-5p/SEMA7A axis facilitated pancreatic cancer progression, which may be regarded as an innovative therapeutic target for PC treatment.Significance of the study: Our findings constitute the first report to delineate that lncRNA LOXL1-AS1/miR-28-5p/SEMA7A axis facilitates PC progression. According to our experimental results, we found the expression of miR-28-5p was downregulated in PC cells and miR-28-5p overexpression inhibited cell proliferation and migration in PC. LOXL1-AS1 could sponge miR-28-5p and then upregulate the expression of SEMA7A. Thus, LOXL1-AS1/miR-28-5p/SEMA7A axis facilitated PC progression. This initially proposed point might provide a novel molecular target for PC treatment.

SNHG15 has been suggested to be correlated with clinical progression and prognosis, and function as tumor suppressive long noncoding RNA in thyroid cancer at our previous study. SNHG15 was proposed to be a potential target for miR-510-5p at LncBase Predicted database. Thus, the aim of this study was to explore the relationship between miR-510-5p and SNHG15 in thyroid cancer, and the clinical significance of miR-510-5p in patients with thyroid cancer. In our results, levels of miR-510-5p expression were increased in thyroid cancer tissues and cell lines compared with adjacent normal thyroid tissues and normal thyroid cell line, respectively. There was a statistically negative correlation between SNHG15 expression and miR-510-5p expression in thyroid cancer tissues. Moreover, miR-510-5p directly bound to SNHG15, and negatively regulated SNHG15 expression in thyroid cancer cells. Furthermore, miR-510-5p promoted thyroid cancer cell proliferation, migration, and invasion through suppressing SNHG15. Finally, high miR-510-5p expression was observed in tumor tissues with advanced clinical stage or lymph node metastasis. In conclusion, we provide evidence to support a pivotal role for miR-510-5p in regulating thyroid cancer cell proliferation, migration, and invasion. K E Y W O R D Slong noncoding RNA, microRNA, miR-510, SNHG15, thyroid cancer