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MICAL2 Contributes to Gastric Cancer Cell Proliferation by Promoting YAP Dephosphorylation and Nuclear Translocation
Chenxiang Qi1, Pengxiang Min2, Qianwen Wang1
1Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
Oxidative Medicine and Cellular Longevity
|October 15, 2021
Summary
MICAL2 promotes gastric cancer cell proliferation by increasing reactive oxygen species (ROS) and activating Cdc42, which leads to YAP dephosphorylation and nuclear translocation, impacting patient survival.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Cytoskeletal dynamics are crucial for cell division in proliferating cells.
- MICAL2 is known to regulate cytoskeletal dynamics and generate reactive oxygen species (ROS).
- The role of MICAL2 in gastric cancer proliferation was previously unknown.
Purpose of the Study:
- To investigate the role of MICAL2 in gastric cancer cell proliferation.
- To elucidate the underlying molecular mechanisms involving ROS, Cdc42, and YAP.
Main Methods:
- MICAL2 expression analysis in gastric cancer tissues.
- MICAL2 knockdown and overexpression experiments.
- Cell cycle analysis, protein level detection (CDK6, cyclin D).
- ROS generation assays, YAP phosphorylation ratio measurement.
- Cdc42 activation assays.
- Treatment with ROS scavengers (NAC, tempol).
Main Results:
- MICAL2 was highly expressed in gastric cancer, correlating with poor survival.
- MICAL2 knockdown caused S-phase arrest, reduced proliferation, and decreased CDK6/cyclin D.
- MICAL2 modulated ROS levels and YAP phosphorylation/localization.
- MICAL2 induced Cdc42 activation, which mediated YAP dephosphorylation and nuclear translocation.
- ROS scavengers reversed MICAL2-induced effects on YAP and proliferation.
Conclusions:
- MICAL2 promotes gastric cancer cell proliferation via ROS generation and Cdc42 activation.
- These pathways converge on YAP dephosphorylation and nuclear translocation.
- MICAL2 represents a potential therapeutic target for gastric cancer.
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