MCTS1 promotes the development of lung adenocarcinoma by regulating E2F1 expression
- Cun Gao
- Rui Dong
- Yongmeng Li
- Jinghui Liang
- Hui Tian
Affiliations: Department of Thoracic Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China
- Published online on: May 17, 2021 https://doi.org/10.3892/ol.2021.12792
Copyright: © Gao
et al. This is an open access article distributed under the
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Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer that results in the majority of cancer‑associated mortality. Multiple copies in T‑cell lymphoma‑1 (MCTS1) is an oncogene that is expressed at high levels in several types of cancer tissues. However, its exact role and pathomechanism in the development of LUAD remains unknown. Reverse transcription‑quantitative PCR analysis was performed to detect MCTS1 expression. Immunohistochemistry analysis was performed to detect MCTS1 expression in LUAD tissues and normal tissues. The MTT, colony formation, EdU, flow cytometry, wound healing and Transwell assays were performed to assess the proliferation, apoptosis, migration and invasion of LUAD cells. Western blot analysis was performed to detect protein expression levels. The present study aimed to investigate the effects of MCTS1 on the progression of LUAD and the potential mechanisms underlying its effects. The results demonstrated that MCTS1 expression was upregulated in LUAD tissues and cells, which was associated with an unfavorable outcome in patients with LUAD. MCTS1 knockdown inhibited LUAD progression by suppressing cell viability and motility, and promoting apoptosis. In addition, E2F1 protein expression was attenuated following MCTS1 knockdown. The silencing MCTS1‑induced inhibitory effect on LUAD malignancy was reversed following overexpression of E2F1 by modulating the c‑Myc signaling pathway. Taken together, the results of the present study suggest that MCTS1 facilitates cell proliferation and migration, and suppresses apoptosis of LUAD cells by regulating E2F1 expression and the c‑Myc signaling pathway.