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HOX转录本反义基因间RNA对舌癌转移、上皮-间质转化及Notch信号通路的影响

Effects of HOX transcript antisense intergenic RNA on the metastasis, epithelial-mesenchymal transition, and Notch signaling pathway in tongue cancer.

作者信息

Zhang Yang, Aodeng Gaowa, Liu Pan, Su Weipeng, Zhao Huarong

机构信息

Cancer Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.

出版信息

Transl Cancer Res. 2021 Jan;10(1):520-528. doi: 10.21037/tcr-20-3452.

Abstract

BACKGROUND

To investigate the effects of long non-coding RNA HOX transcript antisense intergenic RNA (lncHOTAIR) on the proliferation and migration of Tca-8113 cells and TSCCA cells, as well as the epithelial-mesenchymal transition (EMT), and Notch signaling pathway. To further explore the role of HOTAIR in the development of tongue cancer.

METHODS

Transfection was performed on Tca8113 cells using siRNA to knock down the expression of HOTAIR. 3-(4, 5-dimethylthiazole-2-yl)-2, 5-diphenyltetrazole-2, 5-diphenyltetrazole-2, bromination method (MTT) was used to determine the proliferation of the experimental group and the control group. And cellular migration and invasion was evaluated using Transwell assay. Western blot analysis was performed to determine the EMT related protein expression, together with the Notch signaling pathway related protein such as Jagged-1, Notch-1, and Hes-1.

RESULTS

The proliferation of cancer cells was inhibited after silencing with small interfering (si)RNA. The invasion and migration of cancer cells was inhibited after silencing with small interfering (si)RNA (P<0.01). The expression of Jagged-1, Notch-1, and Hes-1 protein in the transfected HOTAIR siRNA cells was substantial decreased compared with the control (P<0.05).

CONCLUSIONS

It is possible that lncHOTAIR contributes to the invasion and metastasis of Tca-8113 and TSCCA cells, which may be related to the EMT. There may be an involvement of HOTAIR in the pathogenesis of tongue cancer through modulation of the Notch signaling pathway.

摘要

背景

探讨长链非编码RNA HOX转录本反义基因间RNA(lncHOTAIR)对Tca-8113细胞和TSCCA细胞增殖、迁移以及上皮-间质转化(EMT)和Notch信号通路的影响。进一步探究HOTAIR在舌癌发生发展中的作用。

方法

使用小干扰RNA(siRNA)对Tca8113细胞进行转染,以敲低HOTAIR的表达。采用3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐法(MTT)检测实验组和对照组细胞的增殖情况。利用Transwell实验评估细胞的迁移和侵袭能力。通过蛋白质免疫印迹法检测EMT相关蛋白以及Notch信号通路相关蛋白如Jagged-1、Notch-1和Hes-1的表达。

结果

小干扰RNA沉默后癌细胞增殖受到抑制。小干扰RNA沉默后癌细胞的侵袭和迁移能力受到抑制(P<0.01)。与对照组相比,转染HOTAIR siRNA的细胞中Jagged-1、Notch-1和Hes-1蛋白的表达显著降低(P<0.05)。

结论

lncHOTAIR可能促进Tca-8113和TSCCA细胞的侵袭和转移,这可能与EMT有关。HOTAIR可能通过调节Notch信号通路参与舌癌的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8abb/8798343/16e1b9a17491/tcr-10-01-520-f1.jpg

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