Poster Session A   |   11:45am Expo - Hall A & C   |   Poster ID #334

Overexpression of mutant EZH2 augments the efficacy of anti-PSMA CAR T therapy against prostate cancer

Program:
Academic Research
Category:
Experimental and Molecular Therapeutics
FDA Status:
Not Applicable
CPRIT Grant:
Cancer Site(s):
Prostate
Authors:
Amrita Barua
University of Houston
Aroshi Mitra
University of Houston
Chengtai Yu
University of Houston
Bin He
Houston Methodist
Qin Feng
University of Houston

Introduction

Immunotherapy has transformed the field of cancer therapeutics, with CAR T therapy being one of its major breakthroughs in the past decade. CAR T therapy has seen incredible success in patients with hematological malignancies. However, the same is not seen in solid tumors. CAR T cells face multiple challenges in solid tumors, one of which is persistence. In this study, we developed a novel CAR T therapy against prostate cancer, and further engineered it to express a constitutively active form of EZH2, aiming to improve the persistence of the T cells by regulating their memory phenotype.

Methods

We used retroviral transduction to generate CAR T cells that recognize PSMA, a frequently overexpressed antigen in prostate cancer. EZH2 is a methyltransferase playing a crucial role in the maintenance of the memory phenotype of CAR T cells. This activity is regulated by Akt, as phosphorylation of EZH2 at serine-21 by Akt deactivates EZH2 methyltransferase activity on histone H3. Thus, in these PSMA CAR T cells, we further expressed an Akt-insensitive EZH2 mutant, with the serine-21 mutated to alanine (EZH2-S21A). This EZH2-S21A represents a constitutively active form of EZH2. We then evaluated the efficacy of the CAR T cells using in vitro T cell cytotoxicity assays and in vivo immunocompromised mouse model xenograft experiments.

Results

EZH2-S21A CAR T cells targeting PSMA have shown superior tumor-killing activity both in vitro and in vivo. Using T cell cytotoxicity assays, we found that EZH2-S21A CAR T cells were able to eliminate PSMA-positive prostate cancer cells at a lower E/T (effector to target cell) ratio compared to PSMA-CAR T. These results were also recapitulated in vivo, using NSG mice subcutaneously injected with prostate cancer tumor cells. Upon intravenous injection of CAR T cells, it was found that the EZH2-S21A CAR T eradicated the tumor faster than the control PSMA-CAR T cells.

Conclusion

Our study suggests that by engineering anti-PSMA CAR T cells to express EZH2-S21A, we can significantly enhance the tumor-killing activity of CAR T cells, both in vitro and in vivo. Further work will be performed to evaluate the persistence of these T cells, such as analyzing the memory markers upon repeated stimulation with tumor cells, and re-injecting tumors into mice to evaluate the in vivo efficacy of these T cells in a tumor rechallenge model.