MN1 engraftment drives p16-3MR. (A) Schematic of p16-3MR model. (B) Fluorescent images of p16-3MR–isolated BMSC that have been cultured alone or with lin⁻, MN1, or HoxA9/Meis1 cells for 6 days (n = 3). (C) Flow cytometry analysis of p16-3MR BMSC that have been cultured alone or with lin⁻, MN1, or HoxA9/Meis1 cells for 6 days (n = 3). (D) Western blot analysis of p16-3MR BMSC cultured alone or with MN1 for 6 days. Blots were reprobed with B-actin to confirm sample loading (shown are representative images of 3 blots). (E) Western blot analysis of p16-3MR BMSC cultured alone or with lin⁻, CM from MN1 cells, or MN1 cells. Blots were reprobed with B-actin to confirm sample loading (shown are representative images of 3 blots). (F) 1 × 10⁵ MN1 cells were injected into the tail vein of p16-3MR mice. BM was isolated and analyzed for mouse BMSC (mCD45⁻, mCD31⁻, mTer119⁻, mCD105⁺, and mCD140a⁺) expressing RFP using flow cytometry (n = 5). (G) Flow cytometry analysis of p16-3MR BMSC measuring RFP (F). The Mann-Whitney U test was used to compare between treatment groups (*P < .05). CM, conditioned media; DC, direct contact; HSV-TK, herpes simplex virus-1 thymidine kinase; TW, transwell.