human endometrioid endometrial cancer (ECC) cell lines ECC-1, HEC-1-A, HEC-1-B, RL95-2 transfection with siRNA using Lullaby

A pool of 4 siRNA duplexes (37.5 nM) were reverse transfected into ECC cell lines (ECC-1, HEC-1-A, HEC-1-B, RL95-2) using Lullaby siRNA transfection reagent.

this article demonstrate the high efficiency of Lullaby, siRNA transfection reagent from OZ Biosciences to induce gene silencing in human endometrioid endometrial cell lines.

paper reference: Clin Cancer Res. 2013 May 14.

PI3K pathway dependencies in endometrioid endometrial cancer cell lines.
Weigelt B, Warne P, Lambros M, Reis-Filho J, Downward J.

Abstract

PURPOSE: Endometrioid endometrial cancers (EECs) frequently harbor coexisting mutations in PI3K pathway genes, including PTEN, PIK3CA, PIK3R1, and KRAS. We sought to define the genetic determinants of PI3K pathway inhibitor response in EEC cells, and whether PTEN-mutant EEC cell lines rely on p110β signaling for survival.
EXPERIMENTAL DESIGN: Twenty-four human EEC cell lines were characterized for their mutation profile and activation state of PI3K and MAPK signaling pathway proteins. Cells were treated with pan-class I PI3K, p110α and p110β isoform-specific, allosteric mTOR, mTOR kinase, dual PI3K/mTOR, MEK and RAF inhibitors. RNA interference (RNAi) was employed to assess effects of KRAS silencing in EEC cells.
RESULTS: EEC cell lines harboring PIK3CA and PTEN mutations were selectively sensitive to the pan-class I PI3K inhibitor GDC-0941 and allosteric mTOR inhibitor Temsirolimus, respectively. Subsets of EEC cells with concurrent PIK3CA and/or PTEN and KRAS mutations were sensitive to PI3K pathway inhibition, and only 2/6 KRAS-mutant cell lines showed response to MEK inhibition. KRAS RNAi silencing did not induce apoptosis in KRAS-mutant EEC cells. PTEN-mutant EEC cell lines were resistant to the p110β inhibitors GSK2636771 and AZD6482, and only in combination with the p110α selective inhibitor A66, a decrease in cell viability was observed.
CONCLUSIONS: Targeted pan-PI3K and mTOR inhibition in EEC cells may be most effective in PIK3CA-mutant and PTEN-mutant tumors, respectively, even in a subset of EECs concurrently harboring KRAS mutations. Inhibition of p110β alone may not be sufficient to sensitize PTEN-mutant EEC cells and combination with other targeted agents may be required.

Lullaby^® is the ideal siRNA transfection reagent for gene silencing reaching up to 90% gene silencing. It protects siRNA from extracellular degradation and maintains high viability due to its bio-degradable properties.