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SOX12 Promotes Thyroid Cancer Cell Proliferation and Invasion by Regulating the Expression of POU2F1 and POU3F1
Zhenxi Su1, Wenqing Bao1, Guanghua Yang1
1Department of General Surgery, Shanghai Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Yonsei Medical Journal
|May 27, 2022
Summary
SOX12 overexpression drives thyroid cancer progression by promoting cell growth and migration. Targeting SOX12 and its interaction with POU factors like POU2F1 offers potential for thyroid cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- SOX12 is frequently overexpressed in various cancers.
- Its role in thyroid cancer progression remains largely unexplored.
Purpose of the Study:
- To investigate the biological function and underlying mechanisms of SOX12 in thyroid cancer.
- To explore SOX12 as a potential therapeutic target.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) data for SOX12 expression.
- Immunohistochemistry and qRT-PCR to confirm SOX12 levels in tissues and cells.
- In vitro functional assays (CCK8, wound healing, Transwell) and in vivo xenograft models.
- Western blot analysis and bioinformatic analysis of protein interactions.
Main Results:
- SOX12 expression is significantly elevated in thyroid cancer tissues and cells.
- SOX12 knockdown suppressed cell proliferation, migration, invasion, and tumor growth.
- SOX12 interacts with POU family members, notably POU2F1 and POU3F1, influencing epithelial-mesenchymal transition (EMT).
- Restoring POU2F1 or POU3F1 expression reversed the effects of SOX12 knockdown.
Conclusions:
- SOX12 promotes thyroid cancer progression by regulating EMT and interacting with POU2F1 and POU3F1.
- SOX12 and its interacting POU factors represent promising novel targets for thyroid cancer molecular therapy.
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