Chondromodulin-I suppresses tumorigenesis of human osteosarcoma cells

Abstract

Osteosarcoma is the most common type of bone cancer, and accounts for ~3% of cancers that occurring in children. Chondromodulin‑I (ChM-I) is a 25 kDa glycoprotein that is expressed mainly in cartilage. ChM-I demonstrates anti‑angiogenic activity and has been suggested to inhibit endothelial cells from invading cartilage, and then has been shown to be an inhibitor of tumorigenesis. However, it remains unclear if ChM‑I has any direct anti‑tumorigenesis role on osteosarcoma. Therefore, the present study aimed to identify whether ChM‑I has any direct inhibit effect on human osteosarcoma cells. A bromodeoxyuridine incorporation assay was performed on the Saos‑2 human osteosarcoma cell line treated with or without recombinant human ChM‑I, to evaluate its impact on DNA synthesis. An adenovirus carrier for the expression of ChM‑I was constructed and transfected into tumor cells in vitro to evaluate the effect of ChM‑I on tumor cells. Additionally, ChM‑I was knocked down by using small interfering RNA to downregulate the expression of ChM‑I. Cell invasion, migration and cell‑colony formation assays, and xenograft tumor experiments were performed to evaluate the effects of ChM‑I on tumor cells in vitro and in vivo. The results demonstrated that ChM‑I could suppress DNA synthesis of human osteosarcoma cells, and it also exerted an inhibitory effect on the proliferation and colony formation abilities of human osteosarcoma cells. In addition, ChM‑I inhibited cell invasion and migration in vitro and suppressed osteosarcoma cell growth significantly in vivo. In conclusion, ChM‑I directly suppressed the proliferation and growth of osteosarcoma cells in an anchorage‑independent manner, and may therefore be a promising drug for the treatment of osteosarcoma.

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

“…The role of Chm-1 in cancers is largely unknown. The anti-angiogenic properties of Chm-1 are postulated to inhibit tumour growth, propagation, and metastasis, indicating that loss of Chm-1 function may induce tumorigenesis [42]. Significantly, Chm-1 appears to be implicated in the pathogenesis of the two most common childhood bone tumours, osteosarcoma and Ewing’s sarcoma (ES) [42, 43].…”

“…The anti-angiogenic properties of Chm-1 are postulated to inhibit tumour growth, propagation, and metastasis, indicating that loss of Chm-1 function may induce tumorigenesis [42]. Significantly, Chm-1 appears to be implicated in the pathogenesis of the two most common childhood bone tumours, osteosarcoma and Ewing’s sarcoma (ES) [42, 43]. Chm-1 has been shown to inhibit the growth and proliferation of human osteosarcoma cells in vivo, and to inhibit the invasion and migration of human osteosarcoma cells in vitro [42].…”

“…Significantly, Chm-1 appears to be implicated in the pathogenesis of the two most common childhood bone tumours, osteosarcoma and Ewing’s sarcoma (ES) [42, 43]. Chm-1 has been shown to inhibit the growth and proliferation of human osteosarcoma cells in vivo, and to inhibit the invasion and migration of human osteosarcoma cells in vitro [42]. Further research is necessary to investigate the properties and mechanisms by which Chm-1 could inhibit osteosarcoma tumorigenesis, and to develop the therapeutic potential of Chm-1 for the treatment of osteosarcoma.…”

Prognostic value of LECT2 and relevance to immune infiltration in hepatocellular carcinoma

“…PPI analysis found that LECT2 has the strongest correlation with LECT1, SVIL, FGG, and DDX46. The study of LECT1 on osteosarcoma cells in vivo showed that it inhibited their growth and proliferation (Lin et al, 2017). Knockdown of DDX46 inhibited osteosarcoma cell proliferation and tumor growth in vivo (Jiang et al, 2017).…”