Abstract
BackgroundThe human Obg-like ATPase 1 (OLA1) protein has been reported to play an important role in cancer cell proliferation. The molecular mechanism underlying OLA1 regulated oral metastasis is still unknown. We investigated in this study the regulatory role of OLA1 playing in oral squamous cell metastasis.ResultsA series of in vitro assays were performed in the cells with RNAi-mediated knockdown or overexpression to expound the regulatory function of OLA1 in oral cancer. We found that the endogenous level of OLA1 in a highly metastatic oral squamous cell line was significantly lower than that in low metastatic oral cells as well as in normal oral cells. Escalated expression of OLA1 resulted in a reduced ability of metastasis in highly metastatic cells, and enhanced its sensitivity to the paclitaxel treatment. Further analysis of the EMT markers showed that Snail, Slug, N-cadherin were up-expressed significantly. Meanwhile, E-cadherin was significantly down-regulated in the oral cancer cells with OLA1-knocked down, suggesting that OLA1 inactivated EMT process. Furthermore, we found that OLA1 suppressed oral squamous cell metastasis by suppressing the activity of a TGFβ/SMAD2/EMT pathway.ConclusionOur data suggests that OLA1 may be developed as a potential target for the treatment of oral cancer metastasis.
Highlights
The human Obg-like ATPase 1 (OLA1) protein has been reported to play an important role in cancer cell proliferation
We found that OLA1 is highly expressed in most of cancer, and have no difference between Head and Neck squamous cell carcinoma (HNSC) and its paired normal tissues (Figs. 1a, S1)
In order to investigate the role of OLA1 in oral cancer cells, five oral squamous cell lines were chosen to detect the endogenous level of OLA1
Summary
The human Obg-like ATPase 1 (OLA1) protein has been reported to play an important role in cancer cell proliferation. The molecular mechanism underlying OLA1 regulated oral metastasis is still unknown. We investigated in this study the regulatory role of OLA1 playing in oral squamous cell metastasis. OSCC is a typical oral malignancy ranking at the sixth among all cancer death worldwide, and accounts for 90% of the incidence of OCC [3]. Increasing evidence indicates that epithelial-mesenchymal transition (EMT) plays a crucial role in the metastasis of cancer [15,16,17,18,19]. EMT is an important biological process of malignant cell migration and invasion of epithelial origin
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