Abstract
The long non-coding RNA antisense 1 ADAMTS9-AS1 has been reported to serve as an oncogene or tumor suppressor in several tumors, including colorectal cancer and hepatocellular carcinoma. Nevertheless, the clinical significance and biological behaviors of ADAMTS9-AS1 in glioma still remain unclear. Therefore, the goal of this study was to evaluate the functional roles and potential mechanisms of ADAMTS9-AS1 in glioma cells. Using quantitative real-time polymerase chain reaction analysis, we found that ADAMTS9-AS1 was upregulated in glioma tissues and cells in comparison to corresponding controls. ADAMTS9-AS1 expression level was correlated to tumor size (p = 0.005) and the World Health Organization grade (p = 0.002). Kaplan–Meier analysis and Cox multivariate analysis showed that ADAMTS9-AS1 could serve as an independent prognostic factor affecting the overall survival of glioma patients. Functionally, depletion of ADAMTS9-AS1 significantly suppressed the proliferation, migration, and invasion in glioma cell lines (U251 and U87), as shown through cell counting kit-8 assay, Edu corporation assay, wound healing assay, and transwell assay. Furthermore, we demonstrated that knockdown of ADAMTS9-AS1 suppressed Wnt1, β-catenin, c-myc, and proliferating cell nuclear antigen, while upregulating E-cadherin expression. In conclusion, our data revealed that ADAMTS9-AS1 confers oncogenic function in the progression of glioma, thus targeting ADAMTS9-AS1 might be a promising therapeutic strategy for this disease.
Highlights
Glioma is considered to be the most common primary intracranial tumor type with high mortality and morbidity [1]
Based on the median value as a cut‐off value, glioma patients were classified into the high (n=40) or the low ADAMTS9-AS1 expression groups (n=39)
Cox univariate and multivariate analysis suggested that the level of ADAMTS9-AS1 could serve as an independent prognostic factor affecting the overall survival of glioma patients (Table 2)
Summary
Glioma is considered to be the most common primary intracranial tumor type with high mortality and morbidity [1]. Zhang et al [9] revealed that lncRNA ASB16-AS1 exhibited higher expression levels in glioma tissue samples and its knockdown inhibited the proliferation, invasion, and migration of glioblastoma stem-like cells. Tumor suppressors, including CASC7 [12] and PTENP1 [13], as well as oncogenes, including SNHG16 [14] and PVT1 [15], play essential roles in glioma. Investigation of these reported molecular mechanisms is far from enough and identification of additional candidate biomarkers is still needed
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