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Updated: May 16, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
MicroRNA-30c targets cytoskeleton genes involved in breast cancer cell invasion
Jessica Bockhorn1, Kathy Yee, Ya-Fang Chang
1The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL 60637, USA.
Abstract:
Metastasis remains a significant challenge in treating cancer. A better understanding of the molecular mechanisms underlying metastasis is needed to develop more effective treatments. Here, we show that human breast tumor biomarker miR-30c regulates invasion by targeting the cytoskeleton network genes encoding twinfilin 1 (TWF1) and vimentin (VIM). Both VIM and TWF1 have been shown to regulate epithelial-to-mesenchymal transition. Similar to TWF1, VIM also regulates F-actin formation, a key component of cellular transition to a more invasive mesenchymal phenotype. To further characterize the role of the TWF1 pathway in breast cancer, we found that IL-11 is an important target of TWF1 that regulates breast cancer cell invasion and STAT3 phosphorylation. The miR-30c-VIM/TWF1 signaling cascade is also associated with clinical outcome in breast cancer patients.
Insights
MicroRNA-30c (miR-30c) impacts cancer spread by targeting twinfilin 1 (TWF1) and vimentin (VIM) genes, crucial for cell invasion. This pathway influences breast cancer patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Metastasis is a major obstacle in cancer therapy, necessitating deeper understanding of its molecular drivers.
- Identifying key regulators of cancer cell invasion is critical for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the role of microRNA-30c (miR-30c) in regulating breast cancer cell invasion.
- To elucidate the molecular targets and signaling pathways modulated by miR-30c in breast cancer metastasis.
Main Methods:
- Analysis of miR-30c targeting of cytoskeleton genes, specifically twinfilin 1 (TWF1) and vimentin (VIM).
- Investigation of the functional impact of VIM and TWF1 on epithelial-to-mesenchymal transition (EMT) and F-actin formation.
- Exploration of the TWF1 pathway, including its regulation of Interleukin-11 (IL-11) and STAT3 phosphorylation.
- Correlation of the miR-30c-VIM/TWF1 signaling cascade with clinical outcomes in breast cancer patients.
Main Results:
- miR-30c was identified as a regulator of breast cancer cell invasion by targeting TWF1 and VIM.
- Both VIM and TWF1 were confirmed to play roles in epithelial-to-mesenchymal transition (EMT).
- VIM, similar to TWF1, was shown to regulate F-actin polymerization, a key event in mesenchymal transition.
- The TWF1 pathway was found to regulate breast cancer cell invasion and STAT3 phosphorylation via IL-11.
- The miR-30c-VIM/TWF1 signaling axis demonstrated association with clinical outcomes in breast cancer patients.
Conclusions:
- miR-30c acts as a tumor suppressor by inhibiting invasion through the VIM/TWF1 pathway.
- The miR-30c-VIM/TWF1-IL-11-STAT3 axis represents a novel signaling cascade influencing breast cancer progression and metastasis.
- Targeting this pathway holds potential for improving therapeutic strategies against metastatic breast cancer.
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