1. Academic Validation
  2. LINC01433 targets miR-506-3p to promote the biological progress of nasopharyngeal carcinoma cells

LINC01433 targets miR-506-3p to promote the biological progress of nasopharyngeal carcinoma cells

  • Eur Arch Otorhinolaryngol. 2021 Sep;278(9):3363-3374. doi: 10.1007/s00405-021-06607-w.
Mingguang Zhou 1 Zhihuai Dong 2 Sunhong Hu 2 Mang Xiao 2
Affiliations

Affiliations

  • 1 Department of Otorhinolaryngology Head and Neck Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3, East Qingchun Road, Hangzhou, 310016, Zhejiang Province, China. mingguang_zhoumg@163.com.
  • 2 Department of Otorhinolaryngology Head and Neck Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3, East Qingchun Road, Hangzhou, 310016, Zhejiang Province, China.
Abstract

Purpose: The current study aimed to investigate the role of long intergenic noncoding 01433 (LINC01433) in the proliferation, migration and invasion of nasopharyngeal carcinoma (NPC).

Methods: Real-time quantitative PCR (RT-qPCR) was performed to determine the expressions of LINC01433 and miR-506-3p in NPC samples and cell lines. The effects of LINC01433 on cell proliferation, migration and invasion were measured by CCK-8, wound healing assay and Transwell, respectively. In addition, Pearson correlation analysis, starBase, RNA immunoprecipitation, luciferase assay, Western blot and functional experiments were conducted to detect and confirm the relationship between LINC01433 and miR-506-3p.

Results: LINC01433 level was noticeably elevated in NPC tissues and cell lines. As the expression of LINC01433 in 5-8F cells was the highest in NPC cell lines and the expression of LINC01433 in SUNE1 cells was the lowest, 5-8F and SUNE1 cells were therefore selected as the target cells for following experiments. Furthermore, miR-506-3p was predicted as the target of LINC01433, and the two were negatively correlated with each Other. Interestingly, overexpression of LINC01433 promoted proliferation, migration and invasion of NPC cells, while miR-506-3p reversed such effects of LINC01433. Moreover, LINC01433 silencing had the opposite effects to LINC01433 overexpression. Furthermore, miR-506-3p overexpression inhibited the expressions of MMP2, N-Cadherin, p-PI3K and p-Akt, and promoted the expressions of E-cadherin and TIMP-2, and partially reversed the role of LINC01433 in promoting Cancer development.

Conclusion: The current findings reveal that LINC01433 regulates NPC cell biological progress through miR-506-3p.

Keywords

LINC01433; Migration; Nasopharyngeal carcinoma; Proliferation; miR-506-3p.

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