<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_raon-2019-0051_s_005_w2aab3b8b1b1b7b1aab1c16b1Aa"><h3>Background</h3><p>Endometrial cancer (EC) is one of the most common gynaecological tumours in the worldwide. Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion in EC cells. However, the molecular mechanisms of NEAT1 in EC have not been fully clarified. We conducted this study to reveal the function of NEAT1 in EC tissues and cell lines.</p></sec><sec id="j_raon-2019-0051_s_006_w2aab3b8b1b1b7b1aab1c16b2Aa"><h3>Materials and methods</h3><p>Cancer and adjacent tissues were collected from EC patients. HEC-1A and Ishikawa cells were cultured <italic>in vitro</italic>. NEAT1 expression was downregulated by transfecting small hairpin RNA (shRNA) and miR-144-3p was overexpressed by transfecting miR-144-3p mimics. Cell proliferation was detected by MTT assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assay. A dual-luciferase reporter assay was used to verify the relationship among NEAT1, EZH2, and miR-144-3p. The expression level of EZH2 was measured by Western blot and qPCR.</p></sec><sec id="j_raon-2019-0051_s_007_w2aab3b8b1b1b7b1aab1c16b3Aa"><h3>Results</h3><p>NEAT1 was highly expressed in EC tissues and cells. Knockdown of NEAT1 inhibited the proliferation, migration and invasion of EC cells. Additionally, NEAT1 acted as a ceRNA of miR-144-3p, leading to EZH2 upregulation. Overexpression of miR-144-3p suppressed the proliferation and invasion of EC cells.</p></sec><sec id="j_raon-2019-0051_s_008_w2aab3b8b1b1b7b1aab1c16b4Aa"><h3>Conclusions</h3><p>NEAT1 promotes EC cells proliferation and invasion by regulating the miR-144-3p/EZH2 axis.</p></sec></abstract>

BackgroundEndometrial cancer (EC) is one of the most common gynaecological tumours in the worldwide. Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion in EC cells. However, the molecular mechanisms of NEAT1 in EC have not been fully clarified. We conducted this study to reveal the function of NEAT1 in EC tissues and cell lines.Materials and methodsCancer and adjacent tissues were collected from EC patients. HEC-1A and Ishikawa cells were cultured in vitro. NEAT1 expression was downregulated by transfecting small hairpin RNA (shRNA) and miR-144-3p was overexpressed by transfecting miR-144-3p mimics. Cell proliferation was detected by MTT assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assay. A dual-luciferase reporter assay was used to verify the relationship among NEAT1, EZH2, and miR-144-3p. The expression level of EZH2 was measured by Western blot and qPCR.ResultsNEAT1 was highly expressed in EC tissues and cells. Knockdown of NEAT1 inhibited the proliferation, migration and invasion of EC cells. Additionally, NEAT1 acted as a ceRNA of miR-144-3p, leading to EZH2 upregulation. Overexpression of miR-144-3p suppressed the proliferation and invasion of EC cells.ConclusionsNEAT1 promotes EC cells proliferation and invasion by regulating the miR-144-3p/EZH2 axis.

LncRNA NEAT1 promotes endometrial cancer cell proliferation, migration and invasion by regulating the miR-144-3p/EZH2 axis

Radiology and Oncology

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

BackgroundEndometrial cancer (EC) is one of the most common gynaecological tumours in the worldwide. Long non-coding RNA (lncRNA) nuclear enriched abundant...

LncRNA NEAT1 promotes endometrial cancer cell proliferation, migration and invasion by regulating the miR-144-3p/EZH2 axis

Article Category: Research Article

Publicado en línea: 20 nov 2019

Páginas: 434 - 442

Recibido: 22 may 2019

Aceptado: 21 sept 2019

DOI: https://doi.org/10.2478/raon-2019-0051

© 2019 Wei Wang, Liang Ge, Xiao-Juan Xu, Ting Yang, Yue Yuan, Xiao-Ling Ma, Xue-Hong Zhang, published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.