Abstract | Background: Methods: The expression level of SPRY4-IT1 in NPC cell lines were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) and colony formation assay were used to detect cell proliferation. Wound-healing assay, transwell assay and animal experiment were performed to evaluate the ability of cell migration and metastasis. Cell cycle distribution and apoptosis were determined by flow cytometry. Western blotting and immunofluorescence were employed to identify protein expression. Results: SPRY4-IT1 was significantly up-regulated in several NPC cell lines (6-10B, CNE-2, and HONE-1) compared with human immortalized nasopharyngeal epithelial cell (NP69). Silencing of SPRY4-IT1 inhibited proliferation, migration, and metastasis, and induced significant G2/M phase arrest and apoptosis. Western blotting showed that the expression levels of cell cycle-related proteins ( cyclin B1, cdc2 and p-cdc2) were down-regulated and apoptosis-associated proteins (PARP, cleaved PARP and cleaved caspase-3) were up-regulated after knockdown of SPRY4-IT1. The expression level of E-cadherin was increased and the expression of Vimentin, Snail and Twist1 were decreased after the SPRY4-IT1 knockdown. Conclusion:
lncRNA SPRY4-IT1 played a significant role in NPC proliferation, migration and metastasis, suggesting that SPRY4-IT1 might be a potential therapeutic target for the treatment of NPC.
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Authors | Yanfei Li, Zhenpeng Liao, Rong Wang, Zibin Liang, Zhihe Lin, Shiqi Deng, Lei Chen, Zhigang Liu, Shaoyan Feng |
Journal | PeerJ
(PeerJ)
Vol. 10
Pg. e13221
( 2022)
ISSN: 2167-8359 [Print] United States |
PMID | 35378932
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | ©2022 Li et al. |
Chemical References |
- RNA, Long Noncoding
- Poly(ADP-ribose) Polymerase Inhibitors
|
Topics |
- Animals
- Humans
- RNA, Long Noncoding
(genetics)
- Cell Line, Tumor
- Nasopharyngeal Carcinoma
(genetics)
- Poly(ADP-ribose) Polymerase Inhibitors
- Gene Expression Regulation, Neoplastic
(genetics)
- Cell Proliferation
(genetics)
- Nasopharyngeal Neoplasms
(genetics)
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