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J Cancer Res Ther. 2019;15(4):927-932. doi: 10.4103/jcrt.JCRT_284_19.

Interleukin 10 promotes growth and invasion of glioma cells by up-regulating KPNA 2 in vitro.

Author information

1
Department of Medical, Queen Mary School, Nanchang University, Nanchang, Jiangxi, China.
2
Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
3
Department of Neurosurgery, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, Jiangxi, China.
4
Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong; Department of Neurosurgery, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, Jiangxi, China.

Abstract

Objective:

Glioma is one of the leading causes of death worldwide with high incidence, recurrence, and mortality. Interleukin-10 (IL-10) is a cytokine with dual function in many types of tumors. Although IL-10 is overexpressed and promotes tumor progression in human primary brain tumor, the mechanisms are largely unknown.

Materials and Methods:

Glioma cells were treated with different dosages of IL-10. The cell growth was detected by CCK-8, and the invasion was measured by Transwell. The relative expression of messenger RNAs was detected by quantitative real-time polymerase chain reaction.

Results:

We found that IL-10 treatment significantly enhanced glioma cell growth and invasion. Moreover, KPNA2 was significantly upregulated after treatment with IL-10. By performing knockdown experiments, we found that the glioma cell growth and invasion were significantly declined.

Conclusions:

The results indicated that knockdown of KPNA2 significantly inhibited the growth and invasion of glioma cells. Moreover, IL-10 promotes glioma progression via upregulation of KPNA2. This study will be of important significance and provides a potential target for treatment of patients with glioma.

KEYWORDS:

Cell growth; KPNA2; cell invasion; glioma; interleukin-10

PMID:
31436254
DOI:
10.4103/jcrt.JCRT_284_19
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