lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling Retraction in /10.3892/or.2024.8785

Wei,Wei; Zhao,Xiaoliang; Zhu,Jianquan; Zhang,Lianmin; Chen,Yulong; Zhang,Bin; Li,Yue; Wang,Meng; Zhang,Zhenfa; Wang,Changli

doi:10.3892/or.2019.7302

lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling

Retraction in: /10.3892/or.2024.8785

Authors:
- Wei Wei
- Xiaoliang Zhao
- Jianquan Zhu
- Lianmin Zhang
- Yulong Chen
- Bin Zhang
- Yue Li
- Meng Wang
- Zhenfa Zhang
- Changli Wang
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Affiliations: Department of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China
Published online on: September 5, 2019 https://doi.org/10.3892/or.2019.7302
Pages: 1946-1956
Copyright: © Wei et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The ligand/receptor pair C‑C motif chemokine ligand 20 (CCL20)/C‑C motif chemokine receptor 6 (CCR6) is considered to be highly activated in lung cancer and significantly accelerates lung cancer progression through activation of ERK signaling. In addition, it has been shown that long non‑coding RNA‑u50535 (lncRNA‑u50535) upregulates CCL20 expression and facilitates cancer progression in colorectal cancer (CRC). However, the effects of lncRNA‑u50535 in lung cancer progression and whether lncRNA‑u50535 regulates CCL20/CCR6/ERK signaling in lung cancer remain ill‑defined. Therefore, the aim of the present study was to investigate the effects of lncRNA‑u50535 on CCL20/CCR6/ERK signaling in lung cancer progression. The results demonstrated that lncRNA‑u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells. Knockdown of lncRNA‑u50535 decreased lung cancer cell proliferation and migration, induced G0/G1 phase arrest and promoted cell apoptosis. Western blot and luciferase reporter gene assays demonstrated that lncRNA‑u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA‑u50535 decreased CCL20, CCR6 and p‑ERK levels. The effects of lncRNA‑u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced. Overall, the present study demonstrated that lncRNA‑u50535 may function as an oncogene in lung cancer progression by regulating CCL20/ERK signaling.

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