Tissue resident stem cells produce CCL5 under the influence of cancer cells and thereby promote breast cancer cell invasion.
In the present study, we investigated whether human adipose tissue derived stem cells (hASCs) could enhance tumor invasion and whether these hASCs could be a potential source of CCL5. We observed a significant increase in the number of breast cancer cells that invaded the matrigel when Co-cultured with hASCs. We found that hASCs produce CCL5 in the Co-culture and cancer cell invasion was diminished by an antibody against CCL5. Furthermore, cancer cell invasion in the Co-culture was associated with an elevated level of MMP-9 activity. We conclude that CCL5 plays a crucial role for tumor invasion in the interplay of tissue resident stem cells from the fat tissue and breast cancer cells.
Department of Molecular Pathology, University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, United States.
Severin
S
Pinilla
Eckhard
E
Alt
F J
FJ
Abdul Khalek
Constantin
C
Jotzu
Fabian
F
Muehlberg
Christoph
C
Beckmann
Yao-Hua
YH
Song
D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology*; D001943:Breast Neoplasms / Q000473:pathology*; D045744:Cell Line, Tumor; D018946:Chemokine CCL5 / Q000096:biosynthesis*; D018920:Coculture Techniques; D003094:Collagen; D004338:Drug Combinations; D006801:Humans; D007797:Laminin; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D009361:Neoplasm Invasiveness; D011509:Proteoglycans; D013234:Stem Cells / Q000378:metabolism / Q000502:physiology*
C483024:CCL5 protein, human; D018946:Chemokine CCL5; D004338:Drug Combinations; D007797:Laminin; D011509:Proteoglycans; C059485:matrigel; D003094:Collagen; D020780:Matrix Metalloproteinase 9