posted on 2023-04-04, 01:40authored byYao-Yu Gong, Hongguang Shao, Yu Li, Patricia Brafford, Zachary E. Stine, Jing Sun, Dean W. Felsher, Jordan S. Orange, Steven M. Albelda, Chi V. Dang
<p>Supplementary Fig. S1. CA9 fails to enhance the cytolytic activity of NK-92 cells in vitro. Supplementary Fig. S2. NHE1 enhances in vitro cytotoxicity of NK-92 cells without affecting proliferation or survival. Supplementary Fig. S3. Representative three-dimensional (3D) reconstruction of confocal microscopic images of antibody-activated NK-92. Supplementary Fig. S4. NHE1 increases the protein expression of c-Myc in NK-92 cells. Supplementary Fig. S5. NHE1 enhances in vitro cytotoxicity of NK-92MI. Supplementary Table S1. Nucleotide sequence of codon-optimized, constitutively active human NHE1 cDNA. Supplementary Table S2. Differentially expressed genes between Na+/H+-exchanger 1 (NHE1)-expressing and empty vector NK-92 cells, ranked by log2(fold change).</p>
Funding
Kathleen M. Rotz Lung Cancer Research Fund
HHS | NIH | National Cancer Institute (NCI)
HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
This study demonstrates the feasibility of metabolic engineering immune effector cells to overcome inhibition in the TME, an approach that could enhance the efficacy of adoptive transfer immunotherapy.