Open Access

Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer

Corrigendum in: /10.3892/etm.2022.11365

  • Authors:
    • Xinpeng Li
    • Naxin Yuan
    • Lingdan Lin
    • Lixia Yin
    • Yiqing Qu
  • View Affiliations

  • Published online on: June 8, 2018     https://doi.org/10.3892/etm.2018.6274
  • Pages: 730-738
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Non‑small cell lung cancer (NSCLC) is the most frequent type of human lung cancer; lung cancer is responsible for the highest rates of cancer‑associated mortality in the world. Cysteine‑rich angiogenic inducer‑61 (CYR‑61) has been identified as a tumorigenesis‑, development‑ and metastasis‑related gene, and is reported to enhance proliferation, migration and invasion through hepatocyte growth factor (HGF)‑induced scattering and the metastasis‑inducing HGF/Met signaling pathway in tumor cells and xenograft models. CYR‑61 is a protein that promotes human lung cancer cell metastasis and is closely related to the patient's prognosis in NSCLC. The purpose of the present study was to investigate whether CYR‑61 may serve as a dual potential target for gene therapy of human NSCLC. In the present study, an antibody targeted against CYR‑61 (anti‑CYR‑61) was constructed and the therapeutic effects and underlying mechanism of this antibody in NSCLC cells and mice with NSCLC was investigated. It was observed that NSCLC cell viability, migration and invasion were inhibited while cell apoptosis was induced by the neutralization of CYR‑61 protein by anti‑CYR‑61. Western blotting demonstrated that extracellular signal‑regulated kinase (ERK) and protein kinase B (AKT) expression levels in NSCLC cells were decreased following treatment with anti‑CYR‑61. In addition, it was observed that inhibition of NSCLC cell viability was achieved by the suppression of the epithelial‑mesenchymal transition signaling pathway. ERK and AKT phosphorylation levels were downregulated in NSCLC cells and tumors following anti‑CYR‑61 treatment. Analysis of a murine model indicated that tumor growth was inhibited and tumor metastasis was significantly suppressed (P<0.01) following anti‑CYR‑61 treatment for CYR‑61. In conclusion, CYR‑61 may serve as a potential target for gene therapy for the treatment of human NSCLC.
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August-2018
Volume 16 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Li X, Yuan N, Lin L, Yin L and Qu Y: Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer Corrigendum in /10.3892/etm.2022.11365. Exp Ther Med 16: 730-738, 2018
APA
Li, X., Yuan, N., Lin, L., Yin, L., & Qu, Y. (2018). Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer Corrigendum in /10.3892/etm.2022.11365. Experimental and Therapeutic Medicine, 16, 730-738. https://doi.org/10.3892/etm.2018.6274
MLA
Li, X., Yuan, N., Lin, L., Yin, L., Qu, Y."Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer Corrigendum in /10.3892/etm.2022.11365". Experimental and Therapeutic Medicine 16.2 (2018): 730-738.
Chicago
Li, X., Yuan, N., Lin, L., Yin, L., Qu, Y."Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer Corrigendum in /10.3892/etm.2022.11365". Experimental and Therapeutic Medicine 16, no. 2 (2018): 730-738. https://doi.org/10.3892/etm.2018.6274