Open Access

MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells

  • Authors:
    • Wenjun Liang
    • Ruichen Gao
    • Mingxia Yang
    • Xiaohua Wang
    • Kewei Cheng
    • Xuejun Shi
    • Chen He
    • Yemei Li
    • Yuying Wu
    • Lei Shi
    • Jingtao Chen
    • Xiaowei Yu
  • View Affiliations

  • Published online on: January 17, 2020     https://doi.org/10.3892/ol.2020.11313
  • Pages: 2272-2280
  • Copyright: © Liang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Lung cancer is the most common cancer in males and females and ~40% of lung cancer cases are adenocarcinomas. Previous studies have demonstrated that myristoylated alanine rich protein kinase C substrate (MARCKS) is upregulated in several types of cancer and is associated with poor prognosis in patients with breast cancer. However, its expression level and role in lung adenocarcinoma remain unknown. Therefore, the aim of the present study was to investigate the expression level and biological functions of MARCKS like 1 (MARCKSL1), a member of the MARCKS family, in lung adenocarcinoma. The expression level of MARCKSL1 was examined in human lung adenocarcinoma tissues and cell lines. MARCKSL1‑specific small interfering RNAs effectively suppressed its expression level and significantly inhibited the proliferation, migration and invasion of lung adenocarcinoma cells. Additionally, the role of MARCKSLI in the regulation of metastasis was examined. Silencing MARCKSL1 decreased the expression of the epithelial‑mesenchymal transition (EMT)‑associated proteins E‑cadherin, N‑cadherin, vimentin and snail family transcriptional repressor 2, and decreased the phosphorylation level of AKT. The results obtained in the current study suggested that MARCKSL1 promoted the progression of lung adenocarcinoma by regulating EMT. MARCKSLI may have prognostic value and serve as a novel therapeutic target in lung adenocarcinoma.
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March-2020
Volume 19 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Liang W, Gao R, Yang M, Wang X, Cheng K, Shi X, He C, Li Y, Wu Y, Shi L, Shi L, et al: MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells. Oncol Lett 19: 2272-2280, 2020
APA
Liang, W., Gao, R., Yang, M., Wang, X., Cheng, K., Shi, X. ... Yu, X. (2020). MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells. Oncology Letters, 19, 2272-2280. https://doi.org/10.3892/ol.2020.11313
MLA
Liang, W., Gao, R., Yang, M., Wang, X., Cheng, K., Shi, X., He, C., Li, Y., Wu, Y., Shi, L., Chen, J., Yu, X."MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells". Oncology Letters 19.3 (2020): 2272-2280.
Chicago
Liang, W., Gao, R., Yang, M., Wang, X., Cheng, K., Shi, X., He, C., Li, Y., Wu, Y., Shi, L., Chen, J., Yu, X."MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells". Oncology Letters 19, no. 3 (2020): 2272-2280. https://doi.org/10.3892/ol.2020.11313