TY - JOUR
T1 - Fullerenol inhibits the cross-talk between bone marrow-derived mesenchymal stem cells and tumor cells by regulating MAPK signaling
AU - Nie, Xin
AU - Tang, Jinglong
AU - Liu, Ying
AU - Cai, Rong
AU - Miao, Qing
AU - Zhao, Yuliang
AU - Chen, Chunying
N1 - Funding Information:
This work was supported by the National Science Fund for Distinguished Young Scholars (11425520) and Excellent Young Scholar Program (1622026), the National Natural Science Foundation of China (31571027, U1532122, 21320102003), the Ministry of Science and Technology of China (National Basic Research Program 2016YFA0201600), the Science Fund for Creative Research Groups of the National Natural Science Foundation of China (11621505), and the CAS Key Research Program for Frontier Sciences (QYZDJ-SSW-SLH022).
Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/8
Y1 - 2017/8
N2 - The interaction between bone marrow-derived mesenchymal stem cells (BDMSCs) and tumor cells promotes tumor proliferation and metastasis. We found that 4T1 breast cancer cells induced malignant differentiation of BDMSCs and that BDMSCs also affected the growth and metastasis of 4T1 cells. However, when the interaction between BDMSCs and 4T1 cells was attenuated or blocked by C60(OH)22 nanoparticles, tumor growth and metastasis were significantly suppressed. The suppression of metastasis depended on the activation of MAPK signals in the BDMSCs, whereas the underlying pathways were related to a broad range of extracellular responses and were modulated by the secretion of multiple cytokines. Interestingly, C60(OH)22 regulated the malignantly differentiated BDMSCs via the Erk- and p38-MAPK and its downstream NF-κB signal pathway, but in normal BDMSCs regulation occurred only through Erk- and p38-MAPK and not by NF-κB activation. This study may provide a novel mechanism for C60(OH)22 nanoparticles as an anti-tumor drug.
AB - The interaction between bone marrow-derived mesenchymal stem cells (BDMSCs) and tumor cells promotes tumor proliferation and metastasis. We found that 4T1 breast cancer cells induced malignant differentiation of BDMSCs and that BDMSCs also affected the growth and metastasis of 4T1 cells. However, when the interaction between BDMSCs and 4T1 cells was attenuated or blocked by C60(OH)22 nanoparticles, tumor growth and metastasis were significantly suppressed. The suppression of metastasis depended on the activation of MAPK signals in the BDMSCs, whereas the underlying pathways were related to a broad range of extracellular responses and were modulated by the secretion of multiple cytokines. Interestingly, C60(OH)22 regulated the malignantly differentiated BDMSCs via the Erk- and p38-MAPK and its downstream NF-κB signal pathway, but in normal BDMSCs regulation occurred only through Erk- and p38-MAPK and not by NF-κB activation. This study may provide a novel mechanism for C60(OH)22 nanoparticles as an anti-tumor drug.
KW - 4T1 tumor cells
KW - Bone marrow-derived mesenchymal stem cells
KW - Fullerenol
KW - MAPK signaling
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U2 - 10.1016/j.nano.2017.03.013
DO - 10.1016/j.nano.2017.03.013
M3 - Article
C2 - 28365417
AN - SCOPUS:85020880069
SN - 1549-9634
VL - 13
SP - 1879
EP - 1890
JO - Nanomedicine: Nanotechnology, Biology, and Medicine
JF - Nanomedicine: Nanotechnology, Biology, and Medicine
IS - 6
ER -