Related Experiment Video
Updated: Feb 11, 2026
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
MicroRNA-150 suppresses triple-negative breast cancer metastasis through targeting HMGA2
Wentao Tang1, Pingping Xu1, Hong Wang1
1Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Background:
Growing evidence suggests that miR-150 plays an inhibitory role in various types of cancer. However, the function and underlying mechanisms of miR-150 in triple-negative breast cancer (TNBC) remain unknown.
Patients And Methods:
miR-150 expression was detected by qRT-PCR and ISH in TNBC tumor and adjacent normal breast tissues. miR-150 function was analyzed by wound healing and transwell assay in vitro and mouse lung metastasis model in vivo. mRNA microarray, qRT-PCR, western blotting and luciferase assay were used to identify the target gene of miR-150. HMGA2 over-expression plasmid was co-transfected with miR-150 to study the role of miR-150 through regulating HMGA2.
Results:
We found that miR-150 was down-regulated in TNBC tumor tissues compared to corresponding adjacent, normal breast tissues, and was correlated with decreased lymph-node metastasis. Ectopic expression of miR-150 suppressed TNBC cell migration in vitro and metastasis in vivo. Mechanistic study revealed that miR-150 down-regulates HMGA2 by directly targeting its mRNA. Moreover, the suppression of cell migration caused by miR-150 is relieved by over-expression of HMGA2, suggesting that miR-150 inhibits migration of TNBC cells by down-regulating HMGA2.
Conclusion:
This work indicates that the miR-150/HMGA2 axis may serve as a treatment marker in TNBC.
Insights
MicroRNA-150 (miR-150) is down-regulated in triple-negative breast cancer (TNBC), inhibiting cell migration by targeting HMGA2. This miR-150/HMGA2 pathway may offer a new TNBC treatment marker.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA-150 (miR-150) is implicated in cancer inhibition.
- Its specific role and mechanisms in triple-negative breast cancer (TNBC) are not well understood.
Purpose of the Study:
- To investigate the function and regulatory mechanisms of miR-150 in TNBC.
- To identify potential therapeutic targets within the miR-150 pathway in TNBC.
Main Methods:
- Quantified miR-150 expression in TNBC tissues versus normal tissues using qRT-PCR and ISH.
- Assessed miR-150's impact on cell migration and metastasis in vitro and in vivo.
- Utilized mRNA microarray, qRT-PCR, western blotting, and luciferase assays to identify miR-150 targets.
- Investigated the miR-150-HMGA2 regulatory axis through co-transfection experiments.
Main Results:
- miR-150 expression was significantly lower in TNBC tissues and correlated with reduced lymph-node metastasis.
- Restoring miR-150 expression inhibited TNBC cell migration and metastasis.
- miR-150 directly targets HMGA2 mRNA, leading to its downregulation.
- Overexpression of HMGA2 reversed the suppressive effect of miR-150 on cell migration.
Conclusions:
- The miR-150/HMGA2 axis plays a crucial role in suppressing TNBC cell migration and metastasis.
- This axis represents a potential therapeutic marker for TNBC treatment.
Related Concept Videos
01:22MicroRNAs
01:22MicroRNAs
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...
01:06Scalar and Vector Triple Products
The scalar triple product is the dot product of a vector with the cross product of two vectors....
01:23Negative Regulator Molecules