Dataset Information

Interfering Expression of Chimeric Transcript SEPT7P2-PSPH Promotes Cell Proliferation in Patients with Nasopharyngeal Carcinoma.

ABSTRACT:

Introduction

Nasopharyngeal carcinoma (NPC) is a distinct type of head and neck cancer which is mostly prevalent in southern China. The development of NPC involves accumulation of multiple genetic changes. Chromosomal translocation is always thought to be accompanied with the fusion chimeric products. To data, the role of the fusion chimeric transcript remains obscure.

Materials and methods

We performed RNA sequencing to detect the fusion genes in ten NPC tissues. Sanger sequencing and quantitative RT-PCR were used to measure the level of the fusion chimeric transcript in NPC tissues and cell lines. The functional experiments such as CCK8 assay, colony formation, and migration/invasion were conducted to analyze the role of this transcript in NPC in vitro.

Results

We demonstrated that the chimeric transcript SEPT7P2-PSPH was formed by trans-splicing of adjacent genes in the absence of chromosomal rearrangement and observed in both NPC patients and cell lines in parallel. Low-expression of the SEPT7P2-PSPH chimeric transcript induced the protein expression of PSPH and promoted cell proliferation, metastasis/invasion, and transforming ability in vitro.

Conclusions

Our findings indicate that the chimeric transcript SEPT7P2-PSPH is a product of trans-splicing of two adjacent genes and might be a tumor suppressor gene, potentially having the role of anticancer activity.

SUBMITTER: Wang J

PROVIDER: S-EPMC6463592 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Interfering Expression of Chimeric Transcript <i>SEPT7P2-PSPH</i> Promotes Cell Proliferation in Patients with Nasopharyngeal Carcinoma.

Wang Jing J Xie Guo-Feng GF He Yuan Y Deng Ling L Long Ya-Kang YK Yang Xin-Hua XH Ma Jiang-Jun JJ Gong Rui R Cen Wen-Jian WJ Ye Zu-Lu ZL Zeng Yi-Xin YX Wang Hai-Yun HY Shao Jian-Yong JY

Journal of oncology 20190401

<h4>Introduction</h4>Nasopharyngeal carcinoma (NPC) is a distinct type of head and neck cancer which is mostly prevalent in southern China. The development of NPC involves accumulation of multiple genetic changes. Chromosomal translocation is always thought to be accompanied with the fusion chimeric products. To data, the role of the fusion chimeric transcript remains obscure.<h4>Materials and methods</h4>We performed RNA sequencing to detect the fusion genes in ten NPC tissues. Sanger sequencin ...[more]

PMID: 31057610

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Project description:The authors' previous study revealed that the serum levels of microRNA (miR)-663b are significantly increased in patients with nasopharyngeal carcinoma (NPC), and are associated with NPC progression and poor prognosis. However, the molecular mechanism of underlying NPC growth and metastasis remains unclear. In the present study, quantitative polymerase chain reaction and western blot analyses were performed to examine changes to mRNA and protein expression, respectively. MTT, wound healing and Transwell assays were used to examine cell proliferation, migration and invasion, respectively. Luciferase reporter gene assays were performed to identify target genes of miR-663b. It was demonstrated that miR-663b was significantly upregulated in NPC tissue compared with non-tumor nasopharyngeal epithelial tissue samples. Furthermore, miR-663b expression gradually increased with advancing stages of NPC, with the highest expression being observed in the latest stage IV. The increased expression of miR-663b was associated with advanced clinical stage and lymph node metastasis. In addition, miR-663b expression was increased in NPC cell lines compared with normal nasopharyngeal epithelial NP69 cells. Knockdown of miR-663b resulted in a significant reduction in the proliferation, migration and invasion of NPC CNE1 cells. Tumor suppressor candidate 2 (TUSC2) was identified as a novel target gene of miR-663b. It was further demonstrated that TUSC2 was significantly downregulated in NPC tissue samples and cell lines. miR-663b negatively regulated the expression of TUSC2 at the post-transcriptional level in CNE1 cells. Additionally, inhibition of TUSC2 expression attenuated the suppressive effects of miR-663b downregulation on the proliferation, migration and invasion of CNE1 cells. To the best of our knowledge, this is the first study to demonstrate that miR-663b, which is upregulated in NPC, promotes the proliferation, migration and invasion of NPC cells, partially through the inhibition of TUSC2 expression. Therefore, it is suggested that miR-663b is a promising therapeutic target for the treatment of patients with NPC.