MiR-133b targets Sox9 to control pathogenesis and metastasis of breast cancer.

Abstract

The miR-133b, a commonly recognized muscle-specific miRNA, was reported to be deregulated in many kinds of cancers. However, its potential roles in tumorigenesis remain greatly elusive. Herein, we demonstrate that miR-133b is significantly suppressed in human breast cancer specimens, which is reversely correlated to histological grade of the cancer. Ectopic expression of miR-133b suppresses clonogenic ability and metastasis-relevant traits in vitro, as well as carcinogenesis and pulmonary metastasis in vivo. Further studies have identified Sox9, c-MET, and WAVE2 as direct targets of miR-133b, in which Sox9 contributes to all miR-133b-endowed effects including cell proliferation, colony formation, as well as cell migration and invasion in vitro. Moreover, re-expression of Sox9 reverses miR-133b-mediated metastasis suppression in vivo. Taken together, these findings highlight an important role for miR-133b in the regulation of tumorigenesis and metastatic potential of breast cancer and suggest a potential application of miR-133b in cancer treatment.

• Authors: Qiu-Yu Wang, Ci-Xiang Zhou, Meng-Na Zhan, Jun Tang, Chen-Long Wang, Cheng-Ning Ma, Ming He, Guo-Qiang Chen, Jian-Rong He, Qian Zhao
• Journal: Cell death & disease (Cell Death Dis) Vol. 9 Issue 7 Pg. 752 (07 03 2018) ISSN: 2041-4889 [Electronic] England
• PMID: 29970901 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• MIRN133 microRNA, human
• MicroRNAs
• SOX9 Transcription Factor
• SOX9 protein, human
• Wiskott-Aldrich Syndrome Protein Family
• MET protein, human
• Proto-Oncogene Proteins c-met

Topics

• Breast Neoplasms (genetics, metabolism, pathology)
• Cell Line, Tumor
• Female
• Gene Expression Regulation, Neoplastic (genetics)
• Humans
• In Vitro Techniques
• MicroRNAs (genetics, metabolism)
• Neoplasm Metastasis (genetics, pathology)
• Proto-Oncogene Proteins c-met (genetics, metabolism)
• SOX9 Transcription Factor (genetics, metabolism)
• Wiskott-Aldrich Syndrome Protein Family (genetics, metabolism)