RNA sequencing of mouse CT26 knockout Pd-l1 cells rescued with WT or K262Q Pd-l1

Although membrane-anchored Pd-l1 has been well-studied for its engagement with PD-1 on T cells to evade anti-tumor immunity, whether Pd-l1 regulate oncogenic signaling pathways in tumor cells remains elusive. In this experiment, to further dissect roles of the K262 residue acetylation for Pd-l1 nuclear function, we profiled RNA expression of WT or K262Q mutant mouse Pd-l1 re-expressed in CT26 KO Pd-l1 cells. Methods: Total RNA fromCT26/Vector, CT26/WT or CT26 Pd-l1 KO cells was purified using Qiagen RNeasy mini kit (Qiagen) according to the manufacturer’s instructions. Library preparation and sequenceing analysis were performed by BGI-Hong Kong Co. Ltd. Conclusions: Our study indicates that Pd-l1 acetylation modification may affect its function in nuclear. Total RNA was extracted from CT26 cells for the following genotypes Pd-l1 knockout cells re-expressed wtih control vector; Pd-l1 knockout cells re-expressed wtih wild type (WT) mouse Pd-l1; and Pd-l1 knockout cells re-expressed wtih K262Q mutant mouse Pd-l1. All subclones are retrovirus infected and selected by puromycin to make stable polyclones. Each group has three repeats.