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Obg-like ATPase 1 inhibited oral carcinoma cell metastasis through TGFβ/SMAD2 axis in vitro
Jianzhou Liu1,2, Qing Yang1, Kevin Chen Xiao3
1State Key Laboratory of Fine Chemicals, Department of Pharmaceutical Sciences, School of Chemical Engineering, Dalian University of Technology, Dalian, 116024, China.
Background:
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.
Results:
A 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.
Conclusion:
Our data suggests that OLA1 may be developed as a potential target for the treatment of oral cancer metastasis.
Insights
The Obg-like ATPase 1 (OLA1) protein suppresses oral cancer metastasis by inhibiting the TGFβ/SMAD2/EMT pathway. Lower OLA1 levels correlate with higher metastasis, suggesting OLA1 as a potential therapeutic target.
Area of Science:
- Molecular biology
- Cancer research
- Oncology
Background:
- The Obg-like ATPase 1 (OLA1) protein is implicated in cancer cell proliferation.
- The specific role of OLA1 in oral squamous cell metastasis remains unclear.
Purpose of the Study:
- To investigate the regulatory role of OLA1 in oral squamous cell metastasis.
- To elucidate the molecular mechanisms by which OLA1 influences oral cancer progression.
Main Methods:
- In vitro assays utilizing RNAi-mediated knockdown and overexpression of OLA1 in oral cancer cells.
- Analysis of epithelial-mesenchymal transition (EMT) markers (Snail, Slug, N-cadherin, E-cadherin).
- Investigation of the TGFβ/SMAD2/EMT pathway activity.
Main Results:
- Endogenous OLA1 levels were significantly lower in highly metastatic oral cancer cells compared to low metastatic and normal cells.
- Overexpression of OLA1 reduced metastatic potential and increased sensitivity to paclitaxel.
- OLA1 suppressed EMT by down-regulating Snail, Slug, N-cadherin, and up-regulating E-cadherin.
- OLA1 inhibits oral squamous cell metastasis by suppressing the TGFβ/SMAD2/EMT pathway.
Conclusions:
- OLA1 plays a critical role in suppressing oral squamous cell metastasis.
- OLA1 inactivation of the TGFβ/SMAD2/EMT pathway is a key mechanism.
- OLA1 represents a potential therapeutic target for treating oral cancer metastasis.
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