Role of cytokine signal suppressor 3 in the regulatory mechanism of colon cancer invasion and proliferation.
10.12122/j.issn.1673-4254.2019.01.07
- Author:
Zhu HONG
1
;
Xipeng ZHANG
1
Author Information
1. Department of Anal and Intestinal Surgery, Tianjin Union Medical Center (Nankai University Affiliated Hospital), Tianjin 300121, China.
- Publication Type:Journal Article
- Keywords:
colon cancer;
cytokine signal suppressor 3;
methylation;
proliferation;
regulation mechanism;
tumor invasion
- MeSH:
Cell Line, Tumor;
Cell Proliferation;
Colonic Neoplasms;
etiology;
pathology;
Cytokines;
Demethylation;
Disease Progression;
Humans;
Interleukin-6;
pharmacology;
Neoplasm Invasiveness;
Neoplasm Proteins;
metabolism;
RNA, Small Interfering;
Signal Transduction;
Suppressor of Cytokine Signaling 3 Protein;
genetics;
metabolism;
Transfection
- From:
Journal of Southern Medical University
2019;39(1):43-48
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the expression of cytokine signal suppressor 3 (SOCS3) in colon cancer tissue and the mechanism by which SOCS3 regulates the proliferation and invasion of colon cancer.
METHODS:We collected the specimens of tumor tissues and paired adjacent tissues from 80 patients with colon cancer undergoing radical resection in our hospital between July, 2014 and May, 2017, and the expression of SOCS3 in the tissue samples was analyzed using Western blotting. We also transfected colon cancer cell line SW480 with a SOCS3-overexpressing plasmid or a small interference RNA (siRNA) for SOCS3 knockdown, and the changes in the cell proliferation and invasion capacity were evaluated using CCK-8 assay and Transwell assay, respectively. The effect of demethylation and IL-6 treatment on SOCS3 expression and the proliferation and invasion of SW480 cells were observed.
RESULTS:Colon cancer tissues showed a lowered expression of SOCS3 compared with the adjacent tissues. Over-expression of SOCS3 significantly inhibited while SOCS3 knockdown obviously promoted the proliferation and invasion of SW480 cells . Demethylation treatment up-regulated SOCS3 expression and inhibited the proliferation and invasion capacity of SW480 cells; IL-6 treatment of the cells caused the reverse changes.
CONCLUSIONS:SOCS3 participates in the development and progression of colon cancer and serves as a potential target for colon cancer treatment. In patients with colon cancer, the low expression of SOCS3 possibly as a result of methylation may promote the proliferation and invasion of the cancer cells.
