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ADAR1 silencing-induced HUVEC apoptosis is mediated by FGFR2 under hypoxia stress
Yun Jiang1, Zhancheng Wang1, Xu Chen1
1Department of Cardiology, The Eighth People's Hospital of Shanghai, Shanghai 200233, China, jiang_yun83@hotmail.com.
Background:
The adenosine deaminase acting on RNA 1 (ADAR1) specifically deaminates adenosine to inosine in double-stranded RNA (dsRNA). Emerging evidence indicated that under hypoxia condition, such as tumor microenvironment, ADAR1 level was increased. Interestingly, we found FGFR2 was also increased under hypoxia stress. The purpose of this study was to investigate the regulation mechanism of ADAR1 and the potential role of ADAR1-FGFR2 axis in cell proliferation and apoptosis.
Methods:
Using human umbilical vein endothelial cells as cellular model, we explored the function of ADAR1 in regulating cell survival.
Results:
We found manipulation of FGFR2 activity could override the cellular effect of ADAR1, suggesting FGFR2 could be a potential effector of ADAR1. Moreover, our results revealed that PI3K-Akt pathway was involved in ADAR1-FGFR2 axis-induced cell proliferation.
Conclusion:
In summary, this study supported the notion that ADAR1 could play a role in tumor cell proliferation, which was mediated by FGFR2.
Insights
Adenosine deaminase acting on RNA 1 (ADAR1) promotes tumor cell proliferation by interacting with FGFR2. This ADAR1-FGFR2 axis involves the PI3K-Akt pathway, influencing cell survival under hypoxia.
Area of Science:
- Molecular Biology
- Cancer Research
- Cellular Signaling
Background:
- Adenosine deaminase acting on RNA 1 (ADAR1) deaminates adenosine to inosine in dsRNA.
- ADAR1 and FGFR2 levels increase under hypoxia, common in tumor microenvironments.
Purpose of the Study:
- Investigate ADAR1 regulation mechanisms.
- Explore the role of the ADAR1-FGFR2 axis in cell proliferation and apoptosis.
Main Methods:
- Utilized human umbilical vein endothelial cells as a cellular model.
- Explored ADAR1 function in regulating cell survival.
Main Results:
- FGFR2 activity manipulation affected ADAR1's cellular impact, indicating FGFR2 as a potential effector.
- The PI3K-Akt pathway is implicated in ADAR1-FGFR2 axis-driven cell proliferation.
Conclusions:
- ADAR1 contributes to tumor cell proliferation.
- FGFR2 mediates the role of ADAR1 in tumor cell proliferation.
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