Oncogenic role of epithelial cell transforming sequence 2 in lung adenocarcinoma cells Retraction in /10.3892/etm.2021.10220

Tan,Hongyi; Wang,Xiaoshan; Yang,Xiaogang; Li,Haitao; Liu,Ben; Pan,Pinhua

doi:10.3892/etm.2016.3584

Oncogenic role of epithelial cell transforming sequence 2 in lung adenocarcinoma cells

Retraction in: /10.3892/etm.2021.10220

Authors:
- Hongyi Tan
- Xiaoshan Wang
- Xiaogang Yang
- Haitao Li
- Ben Liu
- Pinhua Pan
View Affiliations

Affiliations: Department of Respiratory Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China, Department of Oncology, The Third Hospital of Changsha, Changsha, Hunan 410015, P.R. China
Published online on: August 10, 2016 https://doi.org/10.3892/etm.2016.3584
Pages: 2088-2094
Copyright: © Tan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Lung adenocarcinoma, which is the most common non-small cell lung cancer, is the leading cause of death from cancer worldwide. Epithelial cell transforming sequence 2 (ECT2) is frequently upregulated and acts as an oncogene in various human cancers. In addition, ECT2 was reported to be upregulated in early stage lung adenocarcinoma. However, the detailed role of ECT2 in mediating the malignant phenotypes of lung adenocarcinoma cells has not previously been elucidated. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were used to examine ECT2 mRNA and protein expression levels, respectively. MTT, wound healing and Transwell assays were conducted to determine cell proliferation, migration and invasion abilities, respectively. In the present study, ECT2 was significantly upregulated in lung adenocarcinoma cell lines (H650, EKVX, HCC4006, HCC827, HCC2935, Hop62 and A549), as compared with a normal lung epithelial cell line (BEAS‑2B). Moreover, knockdown of ECT2, induced by transfection with ECT2 siRNA, significantly inhibited the proliferation of lung adenocarcinoma A549 cells, whereas overexpression of ECT2 enhanced A549 cell proliferation. Furthermore, knockdown of ECT2 expression suppressed the migration and invasion of A549 cells, whereas overexpression of ECT2 enhanced the migration and invasion abilities of A549 cells. Notably, inhibition of ECT2 also suppressed the expression levels of N‑cadherin and vimentin, whereas it enhanced the expression level of E‑cadherin, indicating that ECT2 is associated with the epithelial‑mesenchymal transition in A549 cells. On the contrary, overexpression of ECT2 enhanced the expression levels of N‑cadherin and vimentin, whereas it reduced the expression level of E‑cadherin in A549 cells. In conclusion, the results of the present study suggest that ECT2 has an oncogenic role in lung adenocarcinoma cells. Therefore, ECT2 may be a potential novel target for the treatment of lung adenocarcinoma.

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