Retinoblastoma protein determines aggressiveness in triple-negative breast cancer

Abstract

Evaluation of: Arima Y, Hayashi H, Sasaki M et al. Induction of ZEB by inactivation of RB is a key determinant of the mesenchymal phenotype of breast cancer. J. Biol. Chem. 287(11), 7896–7906 (2012).

Retinoblastoma protein (RB) is one of the most important tumor suppressors and functions in multiple biological pathways that are deregulated during tumor initiation and progression. Epithelial-to-mesenchymal transition (EMT) is a reversible embryonic process by which epithelial cells lose cell–cell contact and polarity, and its aberrant activation can trigger tumor progression and metastasis. Previously, it has been shown that depletion of RB initiates EMT by downregulating the adhesion molecule E-cadherin. The evaluated article suggests that RB inactivation contributes to loss of cell cycle control and also leads to downregulation of the miR-200 family, thereby causing upregulation of ZEB expression and consequently EMT by downregulation of E-cadherin. RB inactivation could be a key event underlying the mesenchymal and aggressive phenotype of triple-negative breast cancer. Furthermore, exploring links between RB inactivation and EMT might reveal new therapeutic targets for triple-negative breast cancer.

Keywords::

• EMT
• epithelial-to-mesenchymal transition
• miR-200
• RB
• retinoblastoma protein
• TNBC
• triple-negative breast cancer

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.