MCF10A were transfected with siRNA oligo at a final concentration of 37.5 nM using Lullaby according to the protocol recommendations.
This article demonstrates the high efficiency of Lullaby, a transfection reagent from OZ Biosciences dedicated to siRNA to induce gene silencing into mammary gland epithelial cells.article reference: Nat Cell Biol. 2014 Nov;16(11):1092-104.
ASPP2 controls epithelial plasticity and inhibits metastasis through β-catenin-dependent regulation of ZEB1.
Wang Y, Bu F, Royer C, Serres S, Larkin JR, Soto MS, Sibson NR, Salter V, Fritzsche F, Turnquist C, Koch S, Zak J, Zhong S, Wu G, Liang A, Olofsen PA, Moch H, Hancock DC, Downward J, Goldin RD, Zhao J, Tong X, Guo Y, Lu X.Abstract
Epithelial
to mesenchymal transition (EMT), and the reverse mesenchymal to
epithelial transition (MET), are known examples of epithelial plasticity
that are important in kidney development and cancer metastasis. Here we
identify ASPP2, a haploinsufficient tumour suppressor, p53 activator
and PAR3 binding partner, as a molecular switch of MET and EMT. ASPP2
contributes to MET in mouse kidney in vivo. Mechanistically, ASPP2
induces MET through its PAR3-binding amino-terminus, independently of
p53 binding. ASPP2 prevents β-catenin from transactivating ZEB1,
directly by forming an ASPP2-β-catenin-E-cadherin ternary complex and
indirectly by inhibiting β-catenin's N-terminal phosphorylation to
stabilize the β-catenin-E-cadherin complex. ASPP2 limits the
pro-invasive property of oncogenic RAS and inhibits tumour metastasis in
vivo. Reduced ASPP2 expression results in EMT, and is associated with
poor survival in hepatocellular carcinoma and breast cancer patients.
Hence, ASPP2 is a key regulator of epithelial plasticity that connects
cell polarity to the suppression of WNT signalling, EMT and tumour
metastasis.
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