Hou Chao, Dong Yanli, Du Bo
Department of Stomatology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, People's Republic of China.
Cancer Manag Res. 2020 Dec 22;12:13071-13084. doi: 10.2147/CMAR.S282625. eCollection 2020.
Long intergenic non-protein-coding RNA 00466 () promotes lung adenocarcinoma progression. Nonetheless, the expression and precise roles of in tongue squamous cell carcinoma (TSCC) remains uncertain and warrant further investigation. Hence, the present study aimed to examine the effects on the aggressive TSCC cell characteristics and to elucidate the potential underlying mechanisms.
First, expression in TSCC was determined by reverse transcription-quantitative PCR. Subsequently, cell proliferation, apoptosis, migration, and invasion in vitro, as well as tumor growth in vivo were assessed to examine the effects on TSCC cells.
was upregulated in TSCC. This upregulation was notably associated with shorter overall TSCC patient survival. In vitro experiments indicated that depletion suppressed TSCC cell proliferation, migration and invasion, and promoted apoptosis. An in vivo experiment revealed that downregulation attenuated TSCC tumor growth in vivo. Mechanistic analysis revealed that functions as a microRNA-493 (miR-493) molecular sponge, a miRNA that targets high-mobility group AT-hook 2 () mRNA. upregulated HMGA2 in TSCC cells, and this phenomenon was regulated by the miR-493 sponge. Rescue experiments revealed a decrease in the miR-493/HMGA2 axis output, partially reversing the effects of downregulation on aggressive TSCC cell behavior.
These findings demonstrate that promotes TSCC cell oncogenicity in vitro and in vivo by upregulating the miR-493/HMGA2 axis output. These results may provide a new perspective and new insight into the molecular mechanisms of TSCC.
长链基因间非编码RNA 00466()促进肺腺癌进展。然而,其在舌鳞状细胞癌(TSCC)中的表达及确切作用仍不明确,值得进一步研究。因此,本研究旨在探讨对TSCC细胞侵袭性特征的影响,并阐明潜在的作用机制。
首先,通过逆转录定量PCR检测TSCC中的表达。随后,评估体外细胞增殖、凋亡、迁移和侵袭以及体内肿瘤生长情况,以研究对TSCC细胞的影响。
在TSCC中表达上调。这种上调与TSCC患者总体生存期缩短显著相关。体外实验表明,敲低可抑制TSCC细胞增殖、迁移和侵袭,并促进细胞凋亡。体内实验显示,下调可减弱TSCC在体内的肿瘤生长。机制分析表明,作为微小RNA - 493(miR - 493)的分子海绵发挥作用,miR - 493靶向高迁移率族AT钩蛋白2()mRNA。在TSCC细胞中上调HMGA2,且这种现象受miR - 493海绵调节。挽救实验显示miR - 493/HMGA2轴输出降低,部分逆转了下调对TSCC侵袭性细胞行为的影响。
这些发现表明,通过上调miR - 493/HMGA2轴输出在体外和体内促进TSCC细胞的致癌性。这些结果可能为TSCC的分子机制提供新的视角和见解。