Long noncoding RNA LINC00930 promotes PFKFB3-mediated tumor glycolysis and cell proliferation in nasopharyngeal carcinoma

Metabolic reprogramming is a hallmark of cancer. However, the roles of long noncoding RNAs (lncRNAs) in cancer metabolism, especially glucose metabolism remain largely unknown. In this study, we identified and functionally characterized a novel metabolism-related lncRNA, LINC00930, which was upregul...

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Published in:Journal of experimental & clinical cancer research 2022-02, Vol.41 (1), p.77-77, Article 77
Main Authors: He, Baoyu, Pan, Hongli, Zheng, Fengque, Chen, Saiqiong, Bie, Qingli, Cao, Jinghe, Zhao, Rou, Liang, Jing, Wei, Li, Zeng, Jianchao, Li, Hui, Cui, Xing, Ding, Yixuan, Chao, Wei, Xiang, Tiantian, Cheng, Yuhe, Qiu, Gui, Huang, Shishun, Tang, Libo, Chang, Jiansheng, Luo, Delan, Yang, Jie, Zhang, Bin
Format: Article
Language:English
Subjects:
Acetates
Analysis
Animals
Antisense RNA
Cancer
Carcinoma
Cell Line, Tumor
Cell Proliferation
Disease Models, Animal
Female
Glucose metabolism
Glycolysis
Glycolysis - genetics
Humans
LINC00930
Mice
Nasopharyngeal carcinoma
Nasopharyngeal Neoplasms - genetics
Nasopharyngeal Neoplasms - pathology
Oncogenes - genetics
PFKFB3
Phosphofructokinase-2 - metabolism
Prognosis
RBBP5/GCN5
RNA, Long Noncoding - genetics
Transfection
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Summary:Metabolic reprogramming is a hallmark of cancer. However, the roles of long noncoding RNAs (lncRNAs) in cancer metabolism, especially glucose metabolism remain largely unknown. In this study, we identified and functionally characterized a novel metabolism-related lncRNA, LINC00930, which was upregulated and associated with tumorigenesis, lymphatic invasion, metastasis, and poor prognosis in nasopharyngeal carcinoma (NPC). Functionally, LINC00930 was required for increased glycolysis activity and cell proliferation in multiple NPC models in vitro and in vivo. Mechanistically, LINC00930 served as a scaffold to recruit the RBBP5 and GCN5 complex to the PFKFB3 promoter and increased H3K4 trimethylation and H3K9 acetylation levels in the PFKFB3 promoter region, which epigenetically transactivating PFKFB3, and thus promoting glycolytic flux and cell cycle progression. Clinically, targeting LINC00930 and PFKFB3 in combination with radiotherapy induced tumor regression. Collectively, LINC00930 is mechanistically, functionally and clinically oncogenic in NPC. Targeting LINC00930 and its pathway may be meaningful for treating patients with NPC.
ISSN:1756-9966
0392-9078
1756-9966
DOI:10.1186/s13046-022-02282-9