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An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
Published on: June 30, 2015
RORα suppresses breast tumor invasion by inducing SEMA3F expression
Gaofeng Xiong1, Chi Wang, B Mark Evers
1Markey Cancer Center, and the Department of Molecular and Biomedical Pharmacology, Surgery, and Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky 40536, USA.
Abstract:
Inactivation of tumor suppressors and inhibitory microenvironmental factors is necessary for breast cancer invasion; therefore, identifying those suppressors and factors is crucial not only to advancing our knowledge of breast cancer, but also to discovering potential therapeutic targets. By analyzing gene expression profiles of polarized and disorganized human mammary epithelial cells in a physiologically relevant three-dimensional (3D) culture system, we identified retinoid orphan nuclear receptor alpha (RORα) as a transcription regulator of semaphorin 3F (SEMA3F), a suppressive microenvironmental factor. We showed that expression of RORα was downregulated in human breast cancer tissue and cell lines, and that reduced mRNA levels of RORα and SEMA3F correlated with poor prognosis. Restoring RORα expression reprogrammed breast cancer cells to form noninvasiveness structures in 3D culture and inhibited tumor growth in nude mice, accompanied by enhanced SEMA3F expression. Inactivation of RORα in nonmalignant human mammary epithelial cells inhibited SEMA3F transcription and impaired polarized acinar morphogenesis. Using chromatin immunoprecipitation and luciferase reporter assays, we showed that transcription of SEMA3F is directly regulated by RORα. Knockdown of SEMA3F in RORα-expressing cancer cells rescued the aggressive 3D phenotypes and tumor invasion. These findings indicate that RORα is a potential tumor suppressor and inhibits tumor invasion by inducing suppressive cell microenvironment.
Insights
Retinoid orphan nuclear receptor alpha (RORα) acts as a tumor suppressor by regulating semaphorin 3F (SEMA3F), inhibiting breast cancer invasion and improving prognosis. Restoring RORα expression reduces tumor growth and enhances SEMA3F levels.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Breast cancer invasion requires inactivating tumor suppressors and microenvironmental factors.
- Identifying these factors is crucial for understanding breast cancer and developing therapies.
Purpose of the Study:
- To identify novel tumor suppressors and microenvironmental factors involved in breast cancer invasion.
- To investigate the role of retinoid orphan nuclear receptor alpha (RORα) and semaphorin 3F (SEMA3F) in breast cancer progression.
Main Methods:
- Analysis of gene expression profiles in 3D culture models of human mammary epithelial cells.
- Chromatin immunoprecipitation and luciferase reporter assays to determine RORα's regulatory role.
- In vivo studies using nude mice to assess tumor growth inhibition.
Main Results:
- RORα was identified as a regulator of SEMA3F, a suppressive microenvironmental factor.
- RORα and SEMA3F expression were downregulated in human breast cancer tissues and correlated with poor prognosis.
- Restoring RORα expression in cancer cells inhibited tumor growth, enhanced SEMA3F, and promoted non-invasive structures.
- RORα directly regulates SEMA3F transcription, and SEMA3F is essential for RORα's tumor-suppressive effects.
Conclusions:
- RORα functions as a tumor suppressor by inducing a suppressive microenvironment via SEMA3F.
- RORα-SEMA3F signaling represents a potential therapeutic target for inhibiting breast cancer invasion.
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