Suppression of Kiss-1 gene inhibits HCT116 human colorectal carcinoma cell migration in vitro via nuclear factor-κB signaling pathway.
- Author:
Shaoqin CHEN
1
;
Xiaobao SU
;
Ji GAO
;
Hongjing HAN
;
Zhihua CHEN
;
Suyong LIN
Author Information
- Publication Type:Journal Article
- MeSH: Cell Movement; Cell Proliferation; Colorectal Neoplasms; pathology; Genetic Vectors; HCT116 Cells; Humans; I-kappa B Kinase; metabolism; Kisspeptins; genetics; Lentivirus; Matrix Metalloproteinase 9; metabolism; NF-kappa B; metabolism; Neoplasm Invasiveness; Signal Transduction; Transfection
- From: Journal of Southern Medical University 2015;35(11):1643-1648
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of Kiss-1 gene suppression on the metastatic capacity of HCT116 human colorectal carcinoma cells in vitro and the involvement of nuclear factor-κB (NF-κB) signaling pathway.
METHODSA recombinant lentiviral vector of Kiss-1 gene pGC-LV-Kiss-1-EGFP or the empty vector was transfected in HCT116 cells. Cell Counting Kit-8 (CCK8) and Transwell chamber assay were used to detect the changes in cell proliferation, invasion and migration ability after the transfection. Western blotting was used to detect the expression of I-κB, the inhibitive protein of NF-κB signal pathway, and the expression of the downstream effector MMP-9 before and after transfection.
RESULTSIn cells over-expressing Kiss-1, I-κB expression increased and MMP-9 expression decreased significantly compared to those in the blank control and vector-transfected cells (P<0.05). Kiss-1 gene over-expression resulted in significant inhibition of HCT116 cell proliferation, invasion, and migration as compared to the control cells (P<0.05).
CONCLUSIONLentivirus-mediated Kiss-1 gene over-expression can inhibit the proliferation, invasion, and migration of HCT116 cells via the NF-B signaling pathway.
