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Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Implications of Axis Inhibition Protein 2 in Breast Cancer Progression
Sung Yong Ahn1,2,3, Chris Hyunchul Jo1,2,3
1Department of Orthopaedic Surgery, SMG-SNU Boramae Medical Center, Seoul National University College of Medicine, Seoul, Republic of Korea; davidahn@snu.ac.kr chrisjo@snu.ac.kr.
Background/Aim:
Although axis inhibition protein 2 (Axin2) has been reported to act as a tumour suppressor, recent findings suggest that it exhibits oncogenic effects by mediating Snail1-induced epithelial-mesenchymal transition (EMT) in breast cancer cells. EMT is a crucial biological process involved in the initiation of metastasis in cancer progression. This study elucidated the biological significance and mechanism of Axin2 in breast cancer using transcriptomic and molecular techniques.
Materials And Methods:
The expression of Axin2 and Snail1 in MDA-MB-231 breast cancer cells was determined by western blotting analysis, and the role of Axin2 in breast cancer tumorigenesis was investigated in xenograft mouse models constructed using pLKO-Tet-shAxin2-transfected triple negative (TN) breast cancer cells. Additionally, the expression levels of EMT markers were determined using qRT-PCR, and clinical data were analysed using Kaplan-Meier (KM) plotter and The Cancer Genome Atlas (TCGA).
Results:
Axin2 knockdown significantly decreased (p<0.001) the proliferation of MDA-MB-231 cells in vitro and attenuated (p<0.05) the tumorigenic potential of the cells in vivo. Moreover, Axin2 knockdown significantly increased the relative mRNA levels of epithelial markers but decreased the expression of mesenchymal markers in MDA-MB-231 cells.
Conclusion:
Axin2 may be involved in the progression of breast cancer, particularly triple-negative breast cancer, through the regulation of Snail1-induced EMT, making it a potential therapeutic target.
Insights
Axis inhibition protein 2 (Axin2) promotes breast cancer progression by mediating Snail1-induced epithelial-mesenchymal transition (EMT). Axin2 knockdown reduces tumor growth and metastasis, identifying it as a potential therapeutic target for triple-negative breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metastasis
Background:
- Axis inhibition protein 2 (Axin2) traditionally viewed as a tumor suppressor.
- Emerging evidence suggests Axin2 promotes oncogenesis via Snail1-induced epithelial-mesenchymal transition (EMT) in breast cancer.
- EMT is critical for initiating cancer metastasis.
Purpose of the Study:
- To elucidate the biological role and mechanism of Axin2 in breast cancer progression.
- To investigate Axin2's involvement in Snail1-mediated EMT.
- To assess Axin2 as a potential therapeutic target.
Main Methods:
- Western blotting to assess Axin2 and Snail1 expression in MDA-MB-231 cells.
- Xenograft mouse models using Axin2-knockdown triple-negative breast cancer cells to evaluate tumorigenesis.
- Quantitative real-time PCR (qRT-PCR) for EMT marker analysis.
- Kaplan-Meier plotter and The Cancer Genome Atlas (TCGA) for clinical data analysis.
Main Results:
- Axin2 knockdown significantly inhibited MDA-MB-231 cell proliferation in vitro and reduced tumor formation in vivo.
- Axin2 knockdown led to increased epithelial marker expression and decreased mesenchymal marker expression.
- These findings suggest Axin2 promotes EMT and tumor progression.
Conclusions:
- Axin2 plays a significant role in breast cancer progression, especially in triple-negative subtypes.
- Axin2 mediates Snail1-induced EMT, contributing to cancer metastasis.
- Axin2 represents a promising therapeutic target for breast cancer treatment.
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