Abstract
Osteosarcoma (OS) is the most frequent primary bone sarcoma and tends to develop pulmonary metastasis. Studies have shown that mesenchymal stem cells (MSCs) are involved in OS growth and metastasis, but the mechanism remains unclear. The aim of the present study was to identify whether homologous MSCs could promote the growth and metastasis of OS in rats with a normal immune system. The OS cell line, UMR-106, which originally derives from a Sprague-Dawley (SD) rat-transplantable osteogenic sarcoma with an osteoblastic phenotype, has a strong carcinogenic capability and a high lung metastasis. Xenotransplanted models of UMR-106 with or without MSCs injected through the tibia (IT) or caudal vein (IV) were established. SD rats were randomly divided into six groups: Control, UMR-106 (IT), MSCs (IV), UMR-106 (IT) + MSCs (IV), UMR-106 (IV) and UMR-106 (IV) + MSCs (IV). Following injection, all rats were sacrificed at week 5, and the volume and quantity of metastatic sarcoma and the serum alkaline phosphatase levels were measured. There was no metastatic sarcoma in the liver, spleen and kidney in all groups. The rats in the MSCs (IV) + UMR-106 (IV) group showed a significantly higher volume and number of pulmonary metastatic tumors than those of the UMR-106 (IV) group. In pulmonary metastatic tissues, MSCs were found in the MSCs (IV) + UMR-106 (IV) group, but not in the UMR-106 (IT) + MSCs (IV) group. Notably, the expression of vascular endothelial growth factor (VEGF) was increased in the MSCs + UMR-106 cells co-culture system. The present study indicated that MSCs can significantly promote the pulmonary metastasis of the rat OS cell line, UMR-106, with a normal immune system, and VEGF was involved in MSC-promoted UMR-106 emergence and growth of pulmonary metastasis.
Highlights
In the global population, metastasis is the most frequent and life‐threatening complication associated with cancer [1]
The present study indicated that mesenchymal stem cells (MSCs) can significantly promote the pulmonary metastasis of the rat OS cell line, UMR‐106, with a normal immune system, and vascular endothelial growth factor (VEGF) was involved in MSC‐promoted UMR‐106 emergence and growth of pulmonary metastasis
It was shown that there were no metastatic tumors in the control group, which were injected with normal saline solution, and that there were no metastatic tumors in the MSC group
Summary
Metastasis is the most frequent and life‐threatening complication associated with cancer [1]. Studies have shown that MSCs promote the growth and pulmonary metastasis of breast cancer and OS [4,5]. Several studies have shown that the injection of MSCs into a vein promoted the metastasis established in subcutaneous or primary sites [6,7]. Subcutaneous inoculation of COS1NR cells followed by intravenous injection of MSCs at weeks 3 and 5 significantly increased the number of lung nodules [9]. MSCs appear to play a significant role in the adaptation of these traits by carcinoma cells, initiating carcinoma cell phenotypes [10].
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