Long intergenic non-protein coding RNA 02570 promotes nasopharyngeal carcinoma progression by adsorbing microRNA miR-4649-3p thereby upregulating both sterol regulatory element binding protein 1, and fatty acid synthase

ABSTRACT

Our previous studies have elucidated a possible connection between long intergenic non-protein coding RNA 2570 (LINC02570) and nasopharyngeal carcinoma (NPC). However, the precise mechanism by which LINC02570 promotes NPC remains unknown. We used quantitative polymerase chain reaction (qPCR) to detect LINC02570 expression in nasopharyngeal cell lines, NPC tissues, and chronic rhinitis tissues. Subcellular LINC02570 localization was confirmed by fluorescence in situ hybridization (FISH). The effects of LINC02570 stable knockdown and overexpression on viabillity, proliferation, migration, and invasion were analyzed using 3-(4,5-Dimethyl-2-Thiazolyl)-2,5-Diphenyl-2-H-Tetrazolium bromide (MTT), a colorimetric focus-formation assay, a wound healing assay, and transwell assays. RNA crosstalk analysis in silico predicted microRNA-4649-3p (miR-4649-3p) binding to LINC02570 or sterol regulatory element binding transcription factor 1 (SREBF1). A dual luciferase reporter assay was used to confirm potential interactions. Sterol regulatory element binding protein 1 (SREBP1) and fatty acid synthase (FASN) expression were detected by western blotting. The results suggest that LINC02570 is upregulated in late clinical stage NPC patients, and promotes NPC progression by adsorbing miR-4649-3p to up-regulate SREBP1 and FASN. This study elucidates a potential chemotherapeutic target involved in lipid metabolism in NPC.

KEYWORDS:

• LINC02570
• nasopharyngeal carcinoma (NPC)
• miR-4649-3p
• SREBP1
• FASN
• progression

Article highlights

1. LINC02570 is frequently overexpressed in late stage NPC, and is associated with poor prognosis.

2. LINC02570 promotes NPC cell progression.

3. LINC02570 adsorbs and sequesters miR-4649-3p.

4. LINC02570 regulates the miR-4649-3p/SREBP1/FASN axis.

Acknowledgements

We are grateful to Professor Sai-Wah Tsao from University of Hong Kong for generously providing the cell lines HK1, C666-1, and NP69, and To Professor Musheng Zeng from Sun Yat-Sen University for kindly providing SUNE-1, 5-8F, and 6-10B, respectively. This study was supported by the National Natural Science Foundation of China (81960493), Natural Science Foundation of Guangxi Province (2015GXNSFAA139166, 2016GXNSFBA380144), Guangxi Science and Technology Base and Talent Project (Guangxi Nasopharyngeal Carcinoma Clinical Medicine Research Center, 2020AC03005), Guangxi Multidisciplinary Collaboration Health Management Talent Small Highland and Construction Project (Guizu-tongzi-2019-85-9), Self Foundation of the Health Department of Guangxi (Z20190671).

Disclosure statement

The authors have no conflicts of interests to declare.

Supplementary material

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Additional information

Funding

This work was supported by the National Natural Science Foundation of China [81960493]; Natural Science Foundation of Guangxi Province [2016GXNSFBA380144]; Natural Science Foundation of Guangxi Province [2015GXNSFAA139166]; Guangxi Multidisciplinary Collaboration Health Management Talent Small Highland and Construction Project [Guizu-tongzi-2019-85-9]; Guangxi Science and Technology Base and Talent Project [2020AC03005]; Self Foundation of the Health Department of Guangxi [Z20190671].