Related Experiment Video
Updated: Mar 22, 2026
Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module
Published on: June 18, 2015
The Vitamin D Analog, MART-10, Attenuates Triple Negative Breast Cancer Cells Metastatic Potential
Kun-Chun Chiang1, Ta-Sen Yeh2, Shin-Cheh Chen3
1General Surgery Department and Zebrafish Center, Chang Gung Memorial Hospital, Chang Gung University, Keelung 20401, Taiwan. robertviolet6292@yahoo.com.tw.
Abstract:
Regarding breast cancer treatment, triple negative breast cancer (TNBC) is a difficult issue. Most TNBC patients die of cancer metastasis. Thus, to develop a new regimen to attenuate TNBC metastatic potential is urgently needed. MART-10 (19-nor-2α-(3-hydroxypropyl)-1α,25(OH)₂D₃), the newly-synthesized 1α,25(OH)₂D₃ analog, has been shown to be much more potent in cancer growth inhibition than 1α,25(OH)₂D₃ and be active in vivo without inducing obvious side effect. In this study, we demonstrated that both 1α,25(OH)₂D₃ and MART-10 could effectively repress TNBC cells migration and invasion with MART-10 more effective. MART-10 and 1α,25(OH)₂D₃ induced cadherin switching (upregulation of E-cadherin and downregulation of N-cadherin) and downregulated P-cadherin expression in MDA-MB-231 cells. The EMT(epithelial mesenchymal transition) process in MDA-MB-231 cells was repressed by MART-10 through inhibiting Zeb1, Zeb2, Slug, and Twist expression. LCN2, one kind of breast cancer metastasis stimulator, was also found for the first time to be repressed by 1α,25(OH)₂D₃ and MART-10 in breast cancer cells. Matrix metalloproteinase-9 (MMP-9) activity was also downregulated by MART-10. Furthermore, F-actin synthesis in MDA-MB-231 cells was attenuated as exposure to 1α,25(OH)₂D₃ and MART-10. Based on our result, we conclude that MART-10 could effectively inhibit TNBC cells metastatic potential and deserves further investigation as a new regimen to treat TNBC.
Insights
A new vitamin D analog, MART-10, effectively inhibits triple-negative breast cancer (TNBC) metastasis. This compound, more potent than 1α,25(OH)₂D₃, shows promise for developing novel TNBC treatment regimens.
Area of Science:
- Oncology
- Endocrinology
- Cell Biology
Background:
- Triple-negative breast cancer (TNBC) poses a significant therapeutic challenge due to its high metastatic potential.
- Developing novel therapeutic strategies to inhibit TNBC metastasis is crucial for improving patient outcomes.
Purpose of the Study:
- To evaluate the efficacy of a novel 1α,25(OH)₂D₃ analog, MART-10, in attenuating the metastatic potential of TNBC cells.
- To investigate the underlying molecular mechanisms by which MART-10 inhibits TNBC cell migration and invasion.
Main Methods:
- In vitro assessment of TNBC cell migration and invasion.
- Analysis of cadherin switching (E-cadherin, N-cadherin, P-cadherin) and EMT markers (Zeb1, Zeb2, Slug, Twist).
- Evaluation of LCN2 expression, MMP-9 activity, and F-actin synthesis in response to MART-10 and 1α,25(OH)₂D₃ treatment.
Main Results:
- Both 1α,25(OH)₂D₃ and MART-10 significantly repressed TNBC cell migration and invasion, with MART-10 demonstrating superior efficacy.
- MART-10 induced E-cadherin upregulation and N-cadherin/P-cadherin downregulation, while inhibiting EMT markers Zeb1, Zeb2, Slug, and Twist.
- For the first time, LCN2, a breast cancer metastasis stimulator, was found to be repressed by MART-10 and 1α,25(OH)₂D₃. MMP-9 activity and F-actin synthesis were also attenuated.
Conclusions:
- MART-10 effectively inhibits TNBC cell metastatic potential through modulation of cadherin expression, EMT pathways, LCN2, MMP-9, and F-actin.
- MART-10 warrants further investigation as a potential therapeutic agent for treating triple-negative breast cancer.
Related Concept Videos
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...
02:30Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...