Abstract
Aberrant expression of FAM64A was correlated with cell proliferation in various cancer types. We examined the expression of FAM64A and the upstream gene miR-493 in OS. The functions of miR-493 were revealed through extensive experiments. We found an increase of FAM64A gene and protein in OS tissues. Overexpression of FAM64A resulted in promoting tumor proliferation, migration, and invasion. The miR-493 targeted and negatively regulated FAM64A. Our data showed that upregulation of FAM64A in OS correlated with poor prognosis.
Highlights
Osteosarcomas are originated from primitive mesenchymal cells and defined as the most prevalent primary solid tumor of the bone
Xu et al found that FAM64A served as a positive regulator of STAT3, which is linked to various cancer types [7]
We discovered the tumorderived miR-493 targeted to FAM64A and regulated the cell growth and metastasis of OS
Summary
Osteosarcomas are originated from primitive mesenchymal cells and defined as the most prevalent primary solid tumor of the bone. CATS (FAM64A) is confirmed to be highly expressed in leukemia, lymphoma, and a range of tumor cell lines. It has been reported that its protein levels have intense relationship with proliferation in both tumor cells and nonmalignant cells. Silencing of FAM64A resulted in decreased proliferation and cell cycle progression of hematopoietic cells [2]. Xu et al found that FAM64A served as a positive regulator of STAT3, which is linked to various cancer types [7]. We tried to find a new mechanism that interacts with FAM64A in OS. We discovered the tumorderived miR-493 targeted to FAM64A and regulated the cell growth and metastasis of OS
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