Journal
CANCER LETTERS
Volume 273, Issue 1, Pages 140-147Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2008.07.034
Keywords
CD147; MCT; Lactate; Glycolysis; Melanoma
Categories
Funding
- National Natural Science Foundation of China
- Program for New Century Excellent Talents at University
- The Hunan Science Fund for Distinguished Young Scholars
- Jiaikai Foundation, Kagoshima, Japan
Ask authors/readers for more resources
Cancer cells require glycolysis for energy; this results in excessive lactate production and secretion. Lactate, the end product of glycolysis, reduces the extracellular pH and contributes to the proliferation, invasiveness, metastasis, and angiogenesis of tumor cells. Our previous results revealed that the over-expressed CD147/basigin plays a critical role in malignant melanoma (MM) invasiveness, metastasis and angiogenesis: CD147 has also been implicated in a specific and strong interaction with monocarboxylate transporters (MCT) 1 and 4 that mediate the transport of lactate. In the present study, we investigated whether CD147/basigin is involved, via its association with MCT1 and 4 to transport lactate, in glycolysis and then contributes to the progression of A375 melanoma cells. A375 cells expressed remarkably higher CD147, MM and 4 and showed increased glycolysis rate compared with normal human melanocytes (NHMC). CD147/basigin co-localized with MCT1 and 4 in the A375 cell membrane. Furthermore, silencing of CD147/basigin in A375 cells by a siRNA clearly abrogated the expression of MCT1 and 4 and their co-localization with CD147/basigin and dramatically decreased the glycolysis rate, extracellular pH, and the production of ATP. Thus, cell proliferation, invasiveness, and VEGF production were significantly decreased by siRNA. These results strongly suggest that highly-expressed CD147 interacts with MCT1 and 4 to promote tumor cell glycolysis, resulting in the progression of MM. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available