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Mol Med Rep. 2018 Apr;17(4):5764-5773. doi: 10.3892/mmr.2018.8616. Epub 2018 Feb 16.

Lentivirus‑mediated MDA7/IL24 expression inhibits the proliferation of hepatocellular carcinoma cells.

Author information

1
Oncology Center, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Abstract

MDA7/IL24 is a member of the IL‑10 gene family that functions as a cytokine. Notably, supra‑physiological endogenous MDA7 levels have been indicated to suppress tumor growth and induce apoptosis in different cancer types. In the present study, MDA7 roles were investigated during the proliferation of hepatocellular carcinoma (HCC) cells and the molecular mechanisms underlying this process. A lentiviral vector expressing MDA7/IL24 (LV‑MDA7/IL24) was constructed and used to infect HCC SMMC‑7721 cells. The expression levels of MDA7/IL24 in these cells were determined using RT‑qPCR and western blot analysis. The effects of LV‑MDA7/IL24 on cell proliferation were analyzed using MTT and colony formation assays. Furthermore, the influence of LV‑MDA7/IL24 on cell apoptosis and cell cycle distribution were detected using flow cytometry. The underlying molecular mechanisms were investigated using microarray and western blot analysis. The expression of MDA7/IL24 was confirmed to be significantly increased in the cells infected with LV‑MDA7/IL24 compared with that the negative‑control infected group. Lentivirus‑mediated MDA7/IL24 expression was found to inhibit HCC cell proliferation and colony formation, and it also induced cell arrest and apoptosis. Microarray analysis and western blotting results indicated that multiple cancer‑associated pathways and oncogenes are regulated by MDA7/IL24, including cell cycle regulatory and apoptosis activation pathway. In conclusion, it was determined that MDA7/IL24 inhibits the proliferation and reduces the tumorigenicity of HCC cells by regulating cell cycle progression and inducing apoptosis, indicating that it may be used as a potential prognostic and therapeutic target in HCC.

PMID:
29484443
PMCID:
PMC5866019
DOI:
10.3892/mmr.2018.8616
[Indexed for MEDLINE]
Free PMC Article

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