Table 1.
A brief summary of the contribution of β-arrestins in breast cancer phenotype as described in recent studies.
| Protein (β-arrestin 1/2) | Expression/functional contribution/localization | References |
|---|---|---|
| βarr1 and βarr2 | Contribute in PAR-2 mediated migration of MDA MB-231 cells via ERK1/2 MAP kinase activation | Ge, Shenoy, Lefkowitz, and DeFea (2004) |
| βarr2 | Significantly reduces morphine-induced cell death in MCF-7 and MDA-MB231 cells via an Akt and caspase-8 pathways | Zhao et al. (2009) |
| βarr1 and βarr2 | Impair LPA-induced migration and invasion of MDA-MB-231 cells via a Ral GTPase mechanism | Li et al. (2009) |
| βarr1 | Comparatively higher expression in ERα + invasive ductal carcinoma compared to invasive ERα – ductal carcinomas | Rezaul et al. (2010) |
| βarr1 | Inhibits the migration of MDA-MB-468 and MDA-MB-231 cells (2011) | Lundgren et al. (2011) |
| βarr2 | Contributes in Kisspeptin-induced EGFR transactivation, and invasion of MDA-MB-231 cells via MMP-9 | Zajac et al. (2011) |
| βarr2 | Overexpression inhibits proliferation and promotes apoptosis of MCF-7 and T-47D cells via GABABR/JNK pathway | Wu, Shan, Zheng, and Pei (2014) |
| βarr2 | Potentially contributes in GPR161-mediated proliferation and migration of MDA-MB-361 cells via IQGAP1 dependent mechanism | Feigin, Xue, Hammell, and Muthuswamy (2014) |
| βarr2 | βarr2 expression correlates with the levels of MDR1-gp in breast tissue samples and contributes to doxorubicin sensitivity in MDA-MB-231 and MCF-7 cells | Jing et al. (2015) |
| βarr2 | Contributes to Kisspeptin-induced invadopodia formation in MDA-MB-231 via ERK1/2 MAP kinase | Goertzen, Dragan, Turley, Babwah, and Bhattacharya (2016) |
| βarr1 | βarr1 is involved in cellular proliferation and migration in TNBC cells, potentially via AMP kinase activation, and their expression is downregulated in TNBC cells; miR-374a-5p targets and regulates βarr1 expression in TNBC cells | Son et al. (2019) |
| βarr1 and βarr2 | Proteomics-based βarr interactome in MCF-7 cells upon PAR2 activation | Parisis et al. (2013) |
Please note that the table is not exhaustive and highlights some of the key examples available in the literature.