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Updated: Nov 20, 2025
Generation of Multicellular Human Primary Endometrial Organoids
Published on: October 4, 2019
ITRAQ-based proteomics analysis of tanshinone IIA on human ectopic endometrial stromal cells of adenomyosis
Yong Luo1,2, Zeng-Ming Li1, Li-Ping Li3
1Key Laboratory of Women's Reproductive Health of Jiangxi Province, Jiangxi Provincial Maternal and Child Health Hospital, Nanchang, 330006, Jiangxi, China.
Purpose:
Adenomyosis is a diffuse or localized disease. Our previous study has indicated that tanshinone IIA (TSIIA) inhibits the proliferation, migration, and induces apoptosis of ectopic endometrial stromal cells (EESCs) of adenomyosis. However, the complex molecular mechanism of TSIIA in adenomyosis remains unclear. The objective of this study was to explore the complex molecular mechanism of TSIIA on EESCs.
Methods:
In our present study, we used the proteomics approach iTRAQ (isobaric tags for relative and absolute quantitation) combined with LC-MS/MS (liquid chromatography-mass spectrometry) to investigate changes in the protein profile of EESCs treated with TSIIA. Differential proteins were analyzed by employing bioinformatics tools and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. In TSIIA treated EESCs, the protein expression levels of TNFRSF10D, PLEKHM1, FECH, and TPM1A were detected by western blotting.
Results:
Quantitative results revealed 267 significantly differential proteins in TSIIA pretreated EESCs. Gene Ontology (GO) analysis presented an overview of dysregulated proteins in the biological process (BP), cell component (CC), and molecular function (MF) categories. Interestingly, we observed that differential proteins in the extracellular matrix (ECM)-receptor interaction pathway and estrogen signaling pathway were all involved in the focal adhesion pathway, which plays essential roles in the TSIIA-mediated inhibition of EESC proliferation and migration. Furthermore, some significantly differential proteins, which may be potential targets for the treatment of adenomyosis in the future, were validated by western blotting.
Conclusions:
Our study provides a useful method to detect the detailed mechanism underlying the efficacy of TSIIA on EESCs.
Insights
Tanshinone IIA (TSIIA) inhibits adenomyosis cell growth by altering protein expression. This study reveals key molecular pathways, including focal adhesion, involved in TSIIA
Area of Science:
- Proteomics and Bioinformatics
- Molecular Biology
- Gynecological Diseases
Background:
- Adenomyosis is a complex gynecological disease.
- Ectopic endometrial stromal cells (EESCs) are key players in adenomyosis.
- Tanshinone IIA (TSIIA) shows potential therapeutic effects on EESCs.
Purpose of the Study:
- To elucidate the complex molecular mechanisms of TSIIA action on EESCs.
- To identify specific protein targets and pathways affected by TSIIA treatment.
- To provide a foundation for novel adenomyosis therapies.
Main Methods:
- Proteomics analysis using iTRAQ (isobaric tags for relative and absolute quantitation) and LC-MS/MS (liquid chromatography-mass spectrometry).
- Bioinformatics analysis including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
- Validation of key protein expression levels by western blotting.
Main Results:
- Identified 267 significantly differentially expressed proteins in TSIIA-treated EESCs.
- Discovered that TSIIA affects proteins involved in extracellular matrix (ECM)-receptor interaction and estrogen signaling pathways.
- Highlighted the crucial role of the focal adhesion pathway in TSIIA-mediated inhibition of EESC proliferation and migration.
Conclusions:
- This study provides a comprehensive proteomic landscape of TSIIA's effects on EESCs.
- The findings reveal that TSIIA exerts its therapeutic effects by modulating critical cellular pathways.
- Identified potential therapeutic targets for adenomyosis treatment.
