Abstract
SRCIN1 (SRC kinase signalling inhibitor 1) is a new tumor suppressor gene. Previous studies showed that SRCIN1 played a tumor suppressor role in the development of lung cancer and breast cancer. However, the role of SRCIN1 in osteosarcoma is still unknown. In this study, we demonstrated that SRCIN1 was downregulated in osteosarcoma cell lines compared with osteoblastic cell line. Moreover, SRCIN1 was downregulated in osteosarcoma tissues compared with the adjacent tissues. Further investigation revealed that overexpression of SRCIN1 inhibited the osteosarcoma cell line MG-63 proliferation. This effect was confirmed by measuring the ki-67 and PCNA expression. SRCIN1 overexpression promoted E-cadherin expression and suppressed N-cadherin, Vimentin and Snail expression, suggesting that SRCIN1 overexpression inhibited EMT of the osteosarcoma cell. In addition, ectopic expression of SRCIN1 inhibited the MG-63 cell colony formation and invasion. These data suggested that SRCIN1 acted as a tumor suppressor gene in the development of osteosarcoma.
Highlights
Osteosarcoma is one of the most common primary bone malignancies in young adults and adolescents, with an estimated 5.6 per million children suffering from osteosarcoma yearly[1,2,3,4]
We demonstrated that SRCIN1 was downregulated in the osteosarcoma cell lines and tissues
The mRNA expression of SRCIN1 was lower in the osteosarcoma cell lines (MG63, U2OS, SAOS-2 and HOS) than in the one osteoblastic cell line (Fig 1B)
Summary
Osteosarcoma is one of the most common primary bone malignancies in young adults and adolescents, with an estimated 5.6 per million children suffering from osteosarcoma yearly[1,2,3,4]. It occurs mostly in long extremity bone and around regions with active bone growth[5,6,7,8]. SRCIN1 (SRC kinase signalling inhibitor 1), named as p140 Cas-associated protein (p140CAP), contains two regions of highly charged amino acids, two proline-rich regions and two coiled-coil domains[17,18,19,20]. Previous studies demonstrated that SRCIN1 played an PLOS ONE | DOI:10.1371/journal.pone.0155518 August 11, 2016
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