Down-regulation of surface fractalkine by RNA interference in B16 melanoma reduced tumor growth in mice.
It is reported that membrane-bound form of CX3CL1/fractalkine (FKN) promotes cell-cell adhesion by binding with its unique receptor CX3CR1, and membrane fractalkine works as an adhesion molecule for the communication between tumor cells and vascular endothelial cells. Here, we show that CX3CL1/fractalkine was expressed on both mouse and human solid tumors, and small interfering RNA-mediated knock down of fractalkine gene inhibited melanoma B16-F0 cells growth in vivo, which was correlated to the decreased angiogenesis around the tumor. Our findings for the first time suggest that membrane fractalkine may possibly promote tumor angiogenesis through its strong cell adhesion function and therefore serves as a potential target of tumors therapy including RNA interference.
Ren
Tong
T
Institute of Immunology, Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, 443 Huangshan Road, Hefei City, Anhui 230027, PR China.
Chen
Qingfeng
Q
Tian
Zhigang
Z
Wei
Haiming
H
D000818:Animals; D045744:Cell Line, Tumor; D002462:Cell Membrane / Q000378:metabolism; D049109:Cell Proliferation; D054428:Chemokine CX3CL1 / Q000235:genetics / Q000378:metabolism*; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D020868:Gene Silencing; D015316:Genetic Therapy / Q000379:methods*; D008545:Melanoma / Q000235:genetics* / Q000628:therapy*; D051379:Mice; D008810:Mice, Inbred C57BL; D034622:RNA Interference
D054428:Chemokine CX3CL1; C515539:Cx3cl1 protein, mouse