Long noncoding RNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) inhibits proliferation and invasion of glioma cells by suppressing the Wnt/β-catenin signaling pathway

Abstract

BackgroundThe dysregulation of long noncoding RNAs (lncRNAs) has been identified in a variety of cancers. An increasing number of studies have found the critical role of lncRNAs in the regulation of cellular processes, such as proliferation, invasion and differentiation. Long noncoding RNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) is a novel lncRNA that was primarily detected in papillary thyroid carcinoma. However, the biological function and molecular mechanism of lncRNA PTCSC3 in glioma are still unknown.MethodsThe expression level of lncRNA PTCSC3 in human microglia and glioma cell lines was examined using quantitative real-time polymerase chain reaction (qRT-PCR). The influence of lncRNA PTCSC3 on cell proliferation were studied using the cell counting kit-8, and cell cycle and apoptosis were analyzed by flow cytometry assays. The migration and invasion abilities were investigated by transwell and wound healing assays. The target genes of lncRNA PTCSC3 were explored by qRT-PCR, immunofluorescence and western blot.ResultsLncRNA PTCSC3 was significantly downregulated in glioma cell lines. The overexpression of lncRNA PTCSC3 suppressed proliferation and induced apoptosis in U87 and U251 cells. Additionally, the overexpression of lncRNA PTCSC3 inhibited the migration and invasion of U87 and U251 cells. Moreover, lncRNA PTCSC3 inhibited the epithelial-mesenchymal transition of U87 cells. The study also demonstrated that LRP6, as a receptor of the Wnt/β-catenin pathway, was a target of lncRNA PTCSC3. By evaluating the expression levels of Axin1, active β-catenin, c-myc, and cyclin D1, the study indicated that lncRNA PTCSC3 inhibited the activation of the Wnt/β-cateninpathway through targeting LRP6.ConclusionsLncRNA PTCSC3 inhibits the proliferation and migration of glioma cells and suppresses Wnt/β-catenin signaling pathway by targeting LRP6. LncRNA PTCSC3 is a potential therapeutic target for treatment of glioma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-017-0813-6) contains supplementary material, which is available to authorized users.

CacyBP/SIP inhibits the migration and invasion behaviors of glioblastoma cells through activating Siah1 mediated ubiquitination and degradation of cytoplasmic p27

“…In glioma, it is reported that CacyBP/SIP is upregulated and plays an important role in promoting cell proliferation (Shi et al, 2014). However, the migration and invasion behaviors of glioma are regulated by multiple signaling pathways Xia et al, 2017). However, we unexpectedly found that CacyBP/SIP exerted a role in inhibiting the glioma cell migration and invasion.…”

lncRNA FAM83H‑AS1 is associated with the prognosis of colorectal carcinoma and promotes cell proliferation by targeting the Notch signaling pathway

“…lncRNAs have been reported to be involved in a variety of biological processes, including tumorigenesis through regulating oncogenes or tumor suppressors at several levels (3)(4)(5)(6)(7)(8)(9)(10)(11)(12). For example, Xia et al (13) demonstrated that long noncoding RNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) inhibited proliferation and invasion of glioma cells by suppressing the Wnt/β-catenin signaling pathway. Su et al (14) illustrated that long noncoding RNA BLACAT1 indicated a poor prognosis of colorectal cancer and affected cell proliferation by epigenetically silencing p15.…”

Pharmacologic Inhibition of β-Catenin With Pyrvinium Inhibits Murine and Human Models of Wilms Tumor

“…This is consistent with studies showing that the canonical Wnt/β-catenin pathway plays an important role in cellular migration and invasion in multiple tumor types including breast, prostate, gastric, hepatocellular, lung, and thyroid carcinoma cells. 45–51 Pyrvinium has been shown to inhibit β-catenin driven gene transcription, but multiple different mechanisms can inhibit the Wnt/β-catenin pathway including interruption of Wnt interaction with the Frizzled/LRP receptor, 45,46,50 decreasing Wnt ligands, 49 abrogating β-catenin degradation, 51 or altering β-catenin’s interaction with transcription factors in the nucleus affecting gene transcription. 48 This suggests that drug targeting could be tested at a variety of different points in the Wnt/β-catenin signalling cascade making this a fruitful future direction in cancer therapy, including in WT.…”