Long non-coding RNA AC026166.2-001 inhibits cell proliferation and migration in laryngeal squamous cell carcinoma by regulating the miR-24-3p/p27 axis

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作者
Zhisen Shen
Wenjuan Hao
Chongchang Zhou
Hongxia Deng
Dong Ye
Qun Li
Lexi Lin
Bing Cao
Junming Guo
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[1] Medical School of Ningbo University,Department of Otorhinolaryngology and Head and Neck Surgery, the Affiliated Lihuili Hospital
[2] Medical School of Ningbo University,Department of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology
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Long non-coding RNA (lncRNA) AC026166.2-001 was found to be down-regulated in laryngeal squamous cell carcinoma (LSCC) tissues and metastatic neck lymph nodes. Decreased AC026166.2-001 was associated with poorer prognosis and may act as a novel biomarker for LSCC patients. In this study, AC026166.2–001 was overexpressed by a lentivirus vector and down-regulated by a small interfering RNA (siRNA). The results of real-time cell analysis (RTCA) and a plate colony formation assay showed that AC026166.2–001 inhibited LSCC cell proliferation and the clone-forming capacity. Cell cycle distribution and related protein changes were measured by flow cytometry. AC026166.2–001 arrested the cell cycle at the G1 phase and induced apoptosis. In addition, AC026166.2–001 decreased cell migration as measured by wound healing assays and transwell migration assays. Moreover, luciferase reporter assay and Western blotting results suggested that AC026166.2–001 acts as a sponge of miR-24-3p and regulates the expression of p27 and cyclin D1. The in vivo results showed that AC026166.2–001 significantly suppressed the growth of LSCC xenografts and promoted apoptosis. We validated the molecular mechanisms underlying AC026166.2–001 in LSCC. This is the first report of AC026166.2–001 acting as a tumor suppressor in LSCC by regulating the miR-24-3p/p27 axis.
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