Supplementary Figures 1-12, Supplementary Tables 1-3 from AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling
Year: 2023
Type: supplementary-materials
Abstract: S1. Generation of MCF-10A isogenic cells via TP53 knockout and AKT1 E17K knock-in. S2. Frequent co-occurrence of AKT1, TP53 and CDH1 mutations in breast cancers. S3. TP53 CRISPR knockout in MCF-10A cells. S4. Phosphorylation of the AKT1 effector PRAS40 was AKT-dependent in MCF-10A p53ko/E17K cells. S5. Immunofluorescence using a pT308 specific AKT1 antibody of MCF-10A cells following lentiviral infection with V5 tagged (V5 tag) wildtype (WT) or E17K mutant AKT1. S6. Knock-in of the AKT1 E17K mutation did not enhance sensitivity to the pan-AKT kinase inhibitor AZD5363 or the allosteric pan-AKT inhibitor MK2206 in 2Dculture conditions. S7. Survey of previously postulated mechanisms for AKT1-mediated inhibition of cell migration in breast cancer cells. S8. CDH1 promoter methylation status in the MCF-10A isogenic cells. S9. β-catenin interacts with the kinase domain of AKT1. S10. Expression of AKT1 E17K decreased phosphorylation of AKT2 in MCF-10A cells. S11. AKT2 knockdown induces E-cadherin expression in MCF-10A p53ko cells. S12. Model of the mechanism of paradoxical inhibition of cell migration by activated AKT1. Table S1. List of oligonucleotide sequences Table S2. List of antibodies Table S3. List of plasmids
Authors: Sizhi Paul Gao, Amber J. Kiliti, Kai Zhang, Naresh Vasani, Ninghui Mao, Emmet Jordan, Hannah C. Wise, Tripti Shrestha Bhattarai, Wenhuo Hu, Madeline Dorso, James A. Rodrigues, Kwanghee Kim, Aphrothiti J. Hanrahan, Pedram Razavi, Brett Carver, Sarat Chandarlapaty, Jorge S. Reis-Filho, Barry S. Taylor, David B. Solit
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
OpenAlex ID: W4362616150