Abstract
Cucurbitacin B (CuB), a natural product, has anti-tumor effects on various cancers. In order to investigate the expression of long non-coding RNAs (lncRNA), we carried out RNA sequencing (RNA-seq) and quantitative PCR (qPCR). The data indicated that CAL27 and SCC9 tongue squamous cell carcinoma (TSCC) cells had reduced expression of X-inactive specific transcript (XIST) after CuB treatment. Moreover, our results showed increased expression of XIST in human tongue cancer. In this study, CuB treatment inhibited proliferation, migration and invasion of SCC9 cells, and induced cellular apoptosis. Interestingly, knockdown of XIST led to inhibition of cell proliferation and induced apoptosis in vitro. In addition, reduced expression of XIST suppressed cell migration and invasion. MicroRNA 29b (miR-29b) was identified as a direct target of XIST. Previous reports indicated that miR-29b regulates p53 protein. Our results suggest that increased expression of miR-29b induces cell apoptosis through p53 protein. The clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (CRISPR/Cas9) system validated the role of XIST knockout in tumor development in vivo. Together, these results suggest that CuB exerts significant anti-cancer activity by regulating expression of XIST via miR-29b.
Highlights
Significant advances have been made in the diagnosis and treatment of tongue squamous cell carcinoma (TSCC), a type of oral cancer, the 5-year overall survival remains low
In order to analyze the viability of SCC9 cells, the Cell Counting Kit-8 (CCK-8) assay was conducted after Cucurbitacin B (CuB) treatment
Our results demonstrated that CuB induced cell apoptosis and inhibited cell growth, migration and invasion in SCC9 cells
Summary
Significant advances have been made in the diagnosis and treatment of TSCC, a type of oral cancer, the 5-year overall survival remains low. There is evidence that the anti-cancer properties of CuB are through regulated cell death by altering cell cycle progression in osteosarcoma cells [2, 3]. CuB has the ability to induce cell apoptosis via the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway across human gastric carcinoma cells [4]. CuB inhibits cell proliferation by XIST Induce Cell Apoptosis regulating focal adhesion kinase/p53 pathways in human cholangiocarcinoma cells [5]. Previous reports indicated that CuB suppresses cell proliferation through lncRNAs and microRNAs (miRNAs) in pancreatic cancer cells [6]. Results from these studies suggest that CuB plays an important role in cancer development
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