长链非编码 RNA MIR31HG 的沉默通过抑制 PI3K/AKT 信号通路促进鼻咽癌细胞增殖并抑制细胞凋亡。
Silencing of lncRNA MIR31HG promotes nasopharyngeal carcinoma cell proliferation and inhibits apoptosis through suppressing the PI3K/AKT signaling pathway.
机构信息
Department of Otorhinolaryngology, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, China.
Department of Radiochemotherapy, Yinzhou Hospital Affiliated to Medical School of Ningbo University, Ningbo City, China.
出版信息
J Clin Lab Anal. 2022 Dec;36(12):e24720. doi: 10.1002/jcla.24720. Epub 2022 Nov 8.
BACKGROUND
MIR31HG has been affirmed to regulate the tumorigenesis of head-neck squamous cell carcinoma (HNSC). This study aims to reveal the function of MIR31HG in nasopharyngeal carcinoma (NPC), which falls into the category of HNSC.
METHODS
MIR31HG expression pattern in HNSC tissues was predicted by starBase. FISH and qRT-PCR were employed to detect MIR31HG expression in NPC tissues and to analyze the association between MIR31HG and clinicopathological features. NPC cell viability, colony formation, and apoptosis were measured by MTT assay, colony formation assay, and flow cytometry. The expressions of protein kinase B (AKT), phosphorylated (p)-AKT, phosphoinositide 3-kinases (PI3K) and p-PI3K in NPC cells were analyzed by Western blot. The correlation between MIR31HG expression and AKT1 mRNA expression was analyzed by The Cancer Genome Atlas and starBase.
RESULTS
MIR31HG was highly expressed in HNSC tissues and NPC tissues. Meanwhile, the association between high MIR31HG expression and aggressive clinicopathological traits was significant in NPC patients at tumor stage III-IV (T3-T4) and in those with lymph node metastasis 1-2 (N1-N2). Silencing of MIR31HG suppressed NPC cell viability and colony formation, promoted apoptosis, and decreased the expressions of p-PI3K, and p-AKT. 740Y-P reversed the above effects of si-MIR31HG on NPC cells. Besides, MIR31HG expression was positively correlated with AKT1 mRNA expression in HNSC patients.
CONCLUSION
MIR31HG silencing promotes NPC cell proliferation and inhibits apoptosis through suppressing the PI3K/AKT signaling pathway.
背景
MIR31HG 已被证实可调节头颈部鳞状细胞癌（HNSC）的肿瘤发生。本研究旨在揭示 MIR31HG 在鼻咽癌（NPC）中的功能，NPC 属于 HNSC 范畴。
方法
starBase 预测 HNSC 组织中 MIR31HG 的表达模式。采用 FISH 和 qRT-PCR 检测 NPC 组织中 MIR31HG 的表达，并分析 MIR31HG 与临床病理特征的关系。通过 MTT 检测、集落形成实验和流式细胞术检测 NPC 细胞活力、集落形成和凋亡。采用 Western blot 检测 NPC 细胞中蛋白激酶 B（AKT）、磷酸化（p）-AKT、磷酸肌醇 3-激酶（PI3K）和 p-PI3K 的表达。通过 The Cancer Genome Atlas 和 starBase 分析 MIR31HG 表达与 AKT1 mRNA 表达的相关性。
结果
MIR31HG 在 HNSC 组织和 NPC 组织中高表达。同时，在 T3-T4 期和 N1-N2 期 NPC 患者中，高 MIR31HG 表达与侵袭性临床病理特征显著相关。沉默 MIR31HG 抑制 NPC 细胞活力和集落形成，促进凋亡，并降低 p-PI3K 和 p-AKT 的表达。740Y-P 逆转了 si-MIR31HG 对 NPC 细胞的上述作用。此外，在 HNSC 患者中，MIR31HG 表达与 AKT1 mRNA 表达呈正相关。
结论
沉默 MIR31HG 通过抑制 PI3K/AKT 信号通路促进 NPC 细胞增殖并抑制凋亡。
Zotero 插件