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本文引用的文献

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Biochem Genet. 2024 Jun;62(3):2117-2133. doi: 10.1007/s10528-023-10541-3. Epub 2023 Oct 20.
2
Cadherin switching in oral squamous cell carcinoma: A clinicopathological study.口腔鳞状细胞癌中的钙黏蛋白转换:一项临床病理研究。
J Oral Biol Craniofac Res. 2023 Jul-Aug;13(4):486-494. doi: 10.1016/j.jobcr.2023.05.001. Epub 2023 May 31.
3
CDH4 inhibits ferroptosis in oral squamous cell carcinoma cells.CDH4 抑制口腔鳞状细胞癌细胞中的铁死亡。
BMC Oral Health. 2023 May 27;23(1):329. doi: 10.1186/s12903-023-03046-3.
4
Characterization of prognostic value and immunological roles of RAB22A in hepatocellular carcinoma.RAB22A 在肝细胞癌中的预后价值和免疫作用特征。
Front Immunol. 2023 Mar 3;14:1086342. doi: 10.3389/fimmu.2023.1086342. eCollection 2023.
5
Tumour Genetic Heterogeneity in Relation to Oral Squamous Cell Carcinoma and Anti-Cancer Treatment.口腔鳞状细胞癌与抗癌治疗相关的肿瘤遗传异质性。
Int J Environ Res Public Health. 2023 Jan 29;20(3):2392. doi: 10.3390/ijerph20032392.
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Funct Integr Genomics. 2023 Jan 27;23(1):49. doi: 10.1007/s10142-022-00953-6.
7
Overexpression of lncRNA HOXA-AS2 promotes the progression of oral squamous cell carcinoma by mediating SNX5 expression.长链非编码 RNA HOXA-AS2 的过表达通过介导 SNX5 的表达促进口腔鳞状细胞癌的进展。
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NUPR1 promotes the proliferation and metastasis of oral squamous cell carcinoma cells by activating TFE3-dependent autophagy.NUPR1 通过激活 TFE3 依赖性自噬促进口腔鳞状细胞癌细胞的增殖和转移。
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[长链非编码RNA SNHG20通过靶向调控miR-520c-3p/途径对人口腔鳞状细胞癌细胞上皮-间质转化和微管形成的影响]

[Effects of LncRNA SNHG20 on epithelial mesenchymal transition and microtubule formation in human oral squamous cell carcinoma cells through targeted regulation of the miR-520c-3p/ pathway].

作者信息

Ma Minying, Chao Xiaoqin, Zhao Yang, Zhao Guoting

机构信息

Department of Stomatology, The Fifth People's Hospital of Qinghai Province & Qinghai Cancer Hospital, Xining 810001, China.

出版信息

Beijing Da Xue Xue Bao Yi Xue Ban. 2025 Feb 18;57(1):26-32. doi: 10.19723/j.issn.1671-167X.2025.01.005.

DOI:10.19723/j.issn.1671-167X.2025.01.005
PMID:39856503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11759804/
Abstract

OBJECTIVE

To investigate the effects of LncRNA SNHG20 on epithelial mesenchymal transition (EMT) and microtubule formation in human oral squamous cell carcinoma (OSCC) cells through targeted regulation of the miR-520c-3p/ pathway.

METHODS

After real-time fluorescence quantitative detection of LncRNA SNHG20, miR-520c-3p, mRNA expression levels in OSCC tissues and cells, dual luciferase reporter assay was used to detect the relationship between the three. OSCC cells were randomly separated into control group, sh-NC group, sh-SNHG20 group, sh-SNHG20+anti NC group, and sh-SNHG20+anti miR-520c-3p group. Western blotting was used to detect the expression of N-cadherin, vimentin, and E-cadherin proteins in the OSCC cells. The morphology of HSC-3 cells was observed under microscope. Changes in the number of microtubules formed were detected. The effect of LncRNA SNHG20 on the growth of OSCC tumors and the expression levels of LncRNA SNHG20, miR-520c-3p and RAB22 A in the transplanted tumors were detected by nude mice tumorigenesis experiment.

RESULTS

LncRNA SNHG20 and mRNA were upregulated in the OSCC tissues and cells, while miR-520c-3p was downregulated ( < 0.05). There were binding sites between LncRNA SNHG20 and miR-520c-3p, RAB22A and miR-520c-3p, which had targeted regulation relationship. Compared with the sh-NC group, the sh-SNHG20 group had fewer stromal like cells, more epithelial like cells, incomplete microtubule structure, and fewer nodules. LncRNA SNHG20, RAB22A, N-Cadherin, and vimentin were downregulated, while miR-520c-3p and E-cadherin were upregulated ( < 0.05). Compared with the sh-SNHG20+anti-NC group, the sh-SNHG20+anti-miR-520c-3p group had a higher number of stromal like cells, a lower number of epithelioid cells, tighter microtubule arrangement, and more microtubule nodules. miR-520c-3p and E-cadherin were downregulated, while RAB22A, N-cadherin, and vimentin were upregulated ( < 0.05). The transplanted tumor of OSCC in sh-SNHG20 group was smaller and lower than that in sh-NC group. The expression levels of LncRNA SNHG20 and RAB22A in the transplanted tumor tissues were lower than those in sh-NC group, and the expression level of miR-520c-3p was higher than that in sh-NC group ( < 0.05).

CONCLUSION

LncRNA SNHG20 promotes epithelial-mesenchymal transition and microtubule formation in human oral squamous cell carcinoma cells by targeting the miR-520c-3p/ pathway. Inhibiting the expression of LncRNA SNHG20 can target and regulate the miR-520c-3p/ pathway to inhibit EMT and microtubule formation in OSCC cells.

摘要

目的

通过靶向调控miR-520c-3p/ 途径,研究长链非编码RNA SNHG20对人口腔鳞状细胞癌(OSCC)细胞上皮间质转化(EMT)和微管形成的影响。

方法

对OSCC组织和细胞中的LncRNA SNHG20、miR-520c-3p、 mRNA表达水平进行实时荧光定量检测后,采用双荧光素酶报告基因检测法检测三者之间的关系。将OSCC细胞随机分为对照组、sh-NC组、sh-SNHG20组、sh-SNHG20+抗NC组和sh-SNHG20+抗miR-520c-3p组。采用蛋白质免疫印迹法检测OSCC细胞中N-钙黏蛋白、波形蛋白和E-钙黏蛋白的表达。在显微镜下观察HSC-3细胞的形态。检测形成的微管数量的变化。通过裸鼠成瘤实验检测LncRNA SNHG20对OSCC肿瘤生长的影响以及移植瘤中LncRNA SNHG20、miR-520c-3p和RAB22 A的表达水平。

结果

LncRNA SNHG20和 mRNA在OSCC组织和细胞中上调,而miR-520c-3p下调(<0.05)。LncRNA SNHG20与miR-520c-3p、RAB22A与miR-520c-3p之间存在结合位点,具有靶向调控关系。与sh-NC组相比,sh-SNHG20组间质样细胞较少,上皮样细胞较多,微管结构不完整,结节较少。LncRNA SNHG20、RAB22A、N-钙黏蛋白和波形蛋白下调,而miR-520c-3p和E-钙黏蛋白上调(<0.05)。与sh-SNHG20+抗NC组相比,sh-SNHG20+抗miR-520c-3p组间质样细胞数量较多,上皮样细胞数量较少,微管排列更紧密,微管结节更多。miR-520c-3p和E-钙黏蛋白下调,而RAB22A、N-钙黏蛋白和波形蛋白上调(<0.05)。sh-SNHG20组OSCC移植瘤较sh-NC组小且低。移植瘤组织中LncRNA SNHG20和RAB22A的表达水平低于sh-NC组,miR-520c-3p的表达水平高于sh-NC组(<0.05)。

结论

LncRNA SNHG20通过靶向miR-520c-3p/ 途径促进人口腔鳞状细胞癌细胞的上皮间质转化和微管形成。抑制LncRNA SNHG20的表达可靶向调控miR-520c-3p/ 途径,抑制OSCC细胞的EMT和微管形成。