Open Access

Long non‑coding RNA TMPO‑AS1 promotes cell proliferation, migration, invasion and epithelial‑to‑mesenchymal transition in gallbladder carcinoma by regulating the microRNA‑1179/E2F2 axis

  • Authors:
    • Zhenghui Sui
    • Xin Sui
  • View Affiliations

  • Published online on: October 29, 2021     https://doi.org/10.3892/ol.2021.13116
  • Article Number: 855
  • Copyright: © Sui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Gallbladder carcinoma (GBC), which is a common tumor of the biliary system, poses a serious threat to human life and health. The present study aimed to investigate the molecular mechanism of the long non‑coding (lnc)RNA thymopoietin antisense transcript 1 (TMPO‑AS1)/microRNA (miRNA/miR)‑1179/E2F transcription factor 2 (E2F2) axis in GBC. The viability, proliferation, migration, invasion and epithelial‑to‑mesenchymal transition (EMT) of GBC cell lines were assessed via the Cell Counting Kit‑8, colony formation, Transwell migration and invasion, immunofluorescence and western blot assays. In the present study, lncRNA TMPO‑AS1 was significantly upregulated in clinical GBC tissues and cell lines, and was highly expressed in stage III+IV patients with GBC compared with stage I+II patients with GBC. In addition, the overall survival rate of patients with low TMPO‑AS1 expression levels was higher than those with high TMPO‑AS1 expression levels. Furthermore, TMPO‑AS1 knockdown inhibited the viability, proliferation, migration, invasion and EMT of GBC cell lines. In addition, miR‑1179 expression was downregulated in clinical GBC tissues and cell lines, and negatively correlated with TMPO‑AS1 expression. The results revealed that miR‑1179 is a target of TMPO‑AS1, which was confirmed via the dual‑luciferase reporter assay and RNA pull‑down analysis. Overexpression of miR‑1179 inhibited the viability, proliferation, migration, invasion and EMT of GBC cell lines. Furthermore, E2F2 was verified as a direct target of miR‑1179 by binding to its 3'‑untranslated region. E2F2 expression was significantly upregulated in clinical GBC tissues and cell lines, and negatively correlated with miR‑1179 expression. Notably, E2F2 knockdown partially hindered the effects of TMPO‑AS1/miR‑1179 on the proliferation and metastasis of GBC cell lines. Taken together, the results of the present study suggest that TMPO‑AS1 potentially plays a tumor‑promoting role in the occurrence and development of GBC, which may be achieved by regulating the miR‑1179/E2F2 axis.
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