Fig 1: Characterization of siCip2a@PML. Representative immunohistochemical (IHC) staining images of Cip2a (A) and PD-L1 (B) in adjacent non-tumor (paracancerous) tissues and OSCC tissues. n = 5. (C) Cip2a mRNA expression levels in primary HNSCC samples (n = 519) versus matched normal oral tissue samples (n = 44) from TCGA cohort (TPM: Transcripts per million). (D) Kaplan-Meier analysis of overall survival in HNSCC patients stratified by high and low Cip2a expression based on TCGA data. (E) WB analysis of PD-1 and PD-1-Flag protein levels in RAW264.7 and PD1-RAW cells. n = 3. (F) CLSM images of PD-1 expression on RAW264.7 and PD1-RAW cells. PD-1 is shown in red, and nuclei were stained with DAPI (blue). n = 3. Scale bar: 5 μm. (G–I) TEM images (G), hydrodynamic diameter distribution (H), and zeta potentials (I) of siCip2a@L, PD1-MM, and siCip2a@PML. n = 3. Scale bar: 50 nm. (J and K) Membrane fusion during siCip2a@PML formation, visualized by CLSM (J) and flow cytometry (K). siCip2a@L and PD1-MM were labeled with DiI (red) and DiO (green), respectively. Scale bar: 10 μm. (L) WB analysis of CD47, CD11b, and PD-1-Flag protein expression in RAW264.7 cells, PD1-MM, and siCip2a@PML. Na⁺/K⁺ ATPase was used as a loading control. (M) SDS-PAGE protein profiles of PD1-MM, siCip2a@PML, and siCip2a@L. (N) Size variation of siCip2a@PML in 10% FBS for 12 h at 37 °C. n = 3. **p < 0.01