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LINC01116 accelerates nasopharyngeal carcinoma progression based on its enhancement on MYC transcription activity.

ABSTRACT: Long noncoding RNAs (lncRNAs) have been demonstrated to be frequently involved in the development of cancers, whereas only a few of them was investigated in nasopharyngeal carcinoma (NPC). Here, we found that LINC01116 was highly expressed in NPC cell lines, and inhibition of LINC01116 notably restrained cell viability, proliferation, and migration in NPC cells. Besides, we unveiled that LINC01116 was mainly distributed in the cytoplasm of NPC cells. Surprisingly, the cytoplasmic LINC01116 could directly interact with the 5'UTR of MYC mRNA, whereas such interaction had no influence on MYC mRNA expression, but facilitated MYC mRNA translation so as to enhance MYC protein level in NPC cells. Moreover, LINC01116 per se had no impact on the transcription of MYC targets but affected their expression through MYC-dependent manner. Furthermore, MYC overexpression offset the suppression of LINC01116 silence on NPC development. In turn, we discovered that MYC could also serve as the transcriptional activator of LINC01116 in NPC cells. By and large, our findings elucidated a LINC01116/MYC feedback loop in accelerating the tumorigenesis of NPC, revealing a promising target to establish novel biomarkers for NPC patients.

SUBMITTER: Xing H

PROVIDER: S-EPMC6943083 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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LINC01116 accelerates nasopharyngeal carcinoma progression based on its enhancement on MYC transcription activity.

Xing Haijie H Sun Hongxia H Du Weiluo W

Cancer medicine 20191108 1

Long noncoding RNAs (lncRNAs) have been demonstrated to be frequently involved in the development of cancers, whereas only a few of them was investigated in nasopharyngeal carcinoma (NPC). Here, we found that LINC01116 was highly expressed in NPC cell lines, and inhibition of LINC01116 notably restrained cell viability, proliferation, and migration in NPC cells. Besides, we unveiled that LINC01116 was mainly distributed in the cytoplasm of NPC cells. Surprisingly, the cytoplasmic LINC01116 could ...[more]

PMID: 31703161

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Project description:BackgroundCircular RNAs play an important role in tumor genesis and progression, but they have not been sufficiently studied in patients with nasopharyngeal carcinoma (NPC).MethodsThe circular RNA, circCAMSAP1, was screened in NPC cells by RNA sequencing analysis. The expression of circCAMSAP1 in NPC tissues was examined by real-time quantitative polymerase chain reaction (RT-qPCR) and in situ hybridization. Wound-healing, transwell, MTT and flow cytometry assays, and nude mouse tumor models were used to explore the effect of circCAMSAP1 on proliferation and metastasis of NPC in vitro or in vivo. The downstream proteins regulated by circCAMSAP1 were screened using mass spectrometry. The interaction between circCAMSAP1 and the SERPINH1 mRNA was identified using the circular RNA immunoprecipitation method and the luciferase reporter assay. The interaction between SERPINH1 and transcription factor c-Myc was verified through Co-immunoprecipitation (Co-IP) and immunofluorescence. The effect of c-Myc on the generation of circCAMSAP1 was examined through RT-qPCR and chromatin immunoprecipitation. Finally, the splicing factors that promote the production of circCAMSAP1 were explored by RT-qPCR and RNA immunoprecipitation (RIP).ResultsWe found that circCAMSAP1 was highly expressed in NPC tissues and promoted NPC proliferation and metastasis. Additionally, circCAMSAP1 promoted SERPINH1 expression through improved SERPINH1 mRNA stability by binding to the 3'-untranslated region (3'UTR) of SERPINH1. Highly expressed SERPINH1 reduced the ubiquitination-degradation rate of c-Myc, causing increased tumorigenesis. Meanwhile, c-Myc, cooperating with splicing factor 10 (SRSF10), could also promote CAMSAP1 pre-mRNA transcription and back-splicing, forming a positive feedback of circCAMSAP1 production, resulting in the proliferation and metastasis of NPC.ConclusionsOur findings revealed that circCAMSAP1 promotes NPC proliferation and metastasis by binding to the 3'UTR of SERPINH1, suggesting that the positive feedback of circCAMSAP1-SERPINH1-c-Myc may serve as a prognostic biomarker or therapeutic target in patients with NPC.

Dataset Information

LINC01116 accelerates nasopharyngeal carcinoma progression based on its enhancement on MYC transcription activity.

Publications

LINC01116 accelerates nasopharyngeal carcinoma progression based on its enhancement on MYC transcription activity.

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