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2015 ; 5
(ä): 12357
Nephropedia Template TP
Tian L
; Li L
; Xing W
; Li R
; Pei C
; Dong X
; Fu Y
; Gu C
; Guo X
; Jia Y
; Wang G
; Wang J
; Li B
; Ren H
; Xu H
Sci Rep
2015[Jul]; 5
(ä): 12357
PMID26202910
show ga
Melanoma is one of the most aggressive skin cancers and is well known for its
high metastatic rate. Studies have shown that epithelial mesenchymal transition
(EMT) is essential for melanoma cell metastasis. However, the molecular
mechanisms underlying EMT are still not fully understood. We have shown that
IRGM1, a member of immunity-related GTPase family that regulates immune cell
motility, is highly expressed by melanoma cells. The current study aimed to
explore whether and how IRGM1 may regulate melanoma cell metastasis. To test
this, we modified IRGM1 expression in B16 melanoma cells. We found that
over-expression of IRGM1 substantially enhanced pulmonary metastasis in vivo. In
keeping with that, knocking-in IRGM1 strongly enhanced while knocking-down IRGM1
impaired B16 cell migration and invasion ability in vitro. Interestingly, we
observed that IRGM1 enhanced F-actin polymerization and triggers epithelial
mesenchymal transition (EMT) through a mechanism involved in PIK3CA mediated Rac1
activation. Together, these data reveals a novel molecular mechanism that
involved in melanoma metastasis.