Sentence examples for migration of chondrosarcoma from inspiring English sources

More recently, RANTES has been shown to enhance the migration of chondrosarcoma cells through increased MMP-3 production [40].

Activation of PI3K-dependent signaling by BMPs has been implicated in the migration of chondrosarcoma and other cells [17], [18].

Insulin-like growth factor 1 (IGF-1) can enhance the migration of chondrosarcoma cells by upregulating integrin expression.

CCL3 (3 100 ng/ml) induced cell migration and wound healing migration of chondrosarcoma cells (JJ012 & SW1353) in a concentration-dependent manner.

Numerous studies indicate that integrin signaling through FAK plays a role in promoting migration of chondrosarcoma cells [ 62, 64– 66, 73, 74, 95].

Among the growth factors, insulin-like growth factor-I (IGF-I) is able to enhance the migration of chondrosarcoma cells by increasing αv β1 integrin expression, through the IGF-I receptor/PI3K/Akt/NF- κB pathway [ 45].

In this study, we observed that CCL3 increases the migration of human chondrosarcoma cells and upregulates the expression of MMP-2.

BMP-2 has been found to act through PI3K/Akt, IKK α/ β, and NF- κB, resulting in increased β1 integrin expression and migration of human chondrosarcoma cells [ 54].

Adiponectin can promote migration of human chondrosarcoma cells by upregulating α2 β1 integrin, via AdipoR-, AMp38-,p38-, IKK α/ β-, and NF- κB-dependent pathways [ 51].

Leptin was shown to regulate the differentiation of the ATDC5 chondrogenic cell line through activation of ERK1/2 [ 21], and to activate the IRS-1/PI3K/Akt pathway to induce migration of human chondrosarcoma cells [ 22].

GDNF has been shown to promote the migration of human chondrosarcoma cells by upregulating αv β3 integrin expression, through activation of the MEK/ERK, IKK α/ β, and NF- κB pathways [ 55].