Abstract
The long non-coding RNA, urothelial carcinoma associated 1 (UCA1) has been demonstrated to play important roles in various types of cancers. This study investigated the functional role of UCA1 in glioma and explored the underlying molecular mechanisms. UCA1 was found to be highly up-regulated in glioma cells, and knock-down of UCA1 inhibited cell growth, invasion and migration, and also induced apoptosis in glioma cells. On the other hand, overexpression of UCA1 promoted cell proliferation, cell invasion and migration in glioma cells. Knock-down of UCA1 suppressed the activity of Wnt/β-catenin signaling, and treatment with lithium chloride restored the inhibitory effect of UCA1 knock-down on cell invasion and migration. More importantly, the aberrant expression of UCA1 was associated with chemo-resistance to cisplatin and temozolomide in glioma cells via interacting with Wnt/β-catenin signaling. In vivo studies showed that overexpression of UCA1 promoted the in vivo tumor growth of U87 cells in the nude mice. Clinically, UCA1 was found to be up-regulated in glioma tissues and higher expression level of UCA1 was correlated with poor survival in patients with glioma. Taken together, our results showed that UCA1 had a functional role in the regulation of glioma cell growth, invasion and migration, and chemo-resistance possibly via Wnt/β-catenin signaling pathway.
Highlights
Glioma is one of the most deadly cancers of the central nervous system, which accounts for about 80% of primary malignant brain tumors [1]
Our results showed that urothelial carcinoma associated 1 (UCA1) had a functional role in the regulation of glioma cell growth, invasion and migration, and chemo-resistance possibly via Wnt/β-catenin signaling pathway
We identified the up-regulation of UCA1 in glioma cell lines, and further functional study showed that UCA1 knock-down inhibited cell growth, cell invasion and migration, and induced cell apoptosis
Summary
Glioma is one of the most deadly cancers of the central nervous system, which accounts for about 80% of primary malignant brain tumors [1]. The treatment for glioma is surgery in combination with chemotherapy [3, 4]. The pathogenesis of glioma, its underlying molecular mechanism, is largely unknown. Studies have found that gene mutation plays important roles in the pathogenesis of glioma [6]. Epigenetic regulation and noncoding RNAs are found to contribute to glioma development [7, 8]. The detailed mechanisms underlying non-coding RNAs in the pathogenesis of glioma are not fully addressed. Understanding the role of non-coding RNAs in glioma will be helpful for us to identify novel therapy for this malignancy
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