Long non‑coding RNA TMCC1‑AS1 predicts poor prognosis and accelerates epithelial‑mesenchymal transition in liver cancer Retraction in /10.3892/ol.2024.14785

Chen,Cheng; Su,Na; Li,Guiying; Shen,Yanfeng; Duan,Xiaoting

doi:10.3892/ol.2021.13034

Long non‑coding RNA TMCC1‑AS1 predicts poor prognosis and accelerates epithelial‑mesenchymal transition in liver cancer

Retraction in: /10.3892/ol.2024.14785

Authors:
- Cheng Chen
- Na Su
- Guiying Li
- Yanfeng Shen
- Xiaoting Duan
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Affiliations: Oncology Department II, Affiliated Hospital of Hebei Engineering University, Handan, Hebei 056000, P.R. China, Department of Nephrology, Affiliated Hospital of Hebei Engineering University, Handan, Hebei 056000, P.R. China
Published online on: September 9, 2021 https://doi.org/10.3892/ol.2021.13034
Article Number: 773
Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Long non‑coding RNA transmembrane and coiled‑coil domain family 1 antisense RNA 1 (TMCC1‑AS1) has been frequently reported to be associated with prognosis in patients with liver cancer (LC). However, the biological role of TMCC1‑AS1 in LC in vitro remains unclear. The expression levels of TMCC1‑AS1 in primary tumor tissues and LC cell lines were determined using reverse transcription‑quantitative PCR. The associations between TMCC1‑AS1 expression and the clinicopathological factors of patients with LC were statistically analyzed using the χ² test. The role of TMCC1‑AS1 in LC prognosis was assessed using Kaplan‑Meier curves and proportional hazards model (Cox) analysis. Cell proliferation was determined by Cell Counting Kit‑8 and colony formation assays. Transwell assays were performed to determine migration and invasion. TMCC1‑AS1 expression was found to be significantly upregulated in LC tissues and cell lines compared with the corresponding controls. High TMCC1‑AS1 expression was associated with advanced TNM stage and lymph node metastasis. Furthermore, high TMCC1‑AS1 expression predicted poor survival in patients with LC. Knockdown of TMCC1‑AS1 significantly inhibited the proliferation, migration and invasion of HepG2 and SNU‑182 cells, while overexpression of TMCC1‑AS1 had the opposite effect in HepG2 and SNU‑182 cells. At the molecular level, downregulation of TMCC1‑AS1 expression resulted in increased E‑cadherin expression and decreased proliferating cell nuclear antigen, Ki67, N‑cadherin and Vimentin expression in HepG2 cells. Overexpression of TMCC1‑AS1 had the opposite effects on these factors in SNU‑182 cells. In conclusion, the present findings indicated that TMCC1‑AS1 might be considered as a novel oncogene, which promotes cell proliferation and migration, and may be a potential therapeutic target for LC.

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