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Research Article

Silencing of Long Non-coding RNA ENST00000606790.1 Inhibits the Malignant Behaviors of Papillary Thyroid Carcinoma through the PI3K/AKT Pathway

, , , , &
Pages 1-9 | Received 28 Dec 2018, Accepted 24 Jul 2020, Published online: 13 Aug 2020
 

ABSTRACT

Purpose

This study aimed to investigate the role and mechanism of lncRNA ENST00000606790.1 (ENST) in promoting the progression of papillary thyroid carcinoma (PTC).

Methods

The expression of ENST in human PTC and normal para-cancerous thyroid (NPTC) tissues or cell lines was determined by RT-qPCR. Cell growth was determined by CCK8 assay. Cell colony formation was determined by cell colony formation assay. Cell cycle analysis was performed by staining cells with PI (Propidium Iodide). Cell invasion was assessed by transwell assay. Protein expression was examined by western-blot. siRNA was constructed to inhibit the expression of ENST. 740-Y-P was used to activate PI3K. The correlation between ENST expression and clinical outcomes was analyzed.

Results

ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively. High expression of ENST was strongly correlated to lymph node metastasis and tumor size at diagnosis. Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion. Silencing of ENST significantly down-regulated the expression of PI3K, p-PI3K, AKT, and p-AKT in IHH4 cells. Furthermore, treatment with the PI3K activator  740-Y-P partially abolished the effect of silencing of ENST on PTC cells.

Conclusions

Overall, our results demonstrated that ENST can promote PTC progression by activating the PI3K/AKT signaling pathway, suggesting that ENST can serve as a potential biomarker and new therapeutic target for patients with PTC.

Disclosure Of Interest

No potential conflicts of interest relevant to this article were reported. The authors alone are responsible for the content and writing of the paper.

Data Availability Statement

The authors confirm that the data supporting the findings of this study are available within the article .

Additional information

Funding

This work was supported by the Key Research and Development Project of Jiangsu Province under [grant BE2015723].

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