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Figure 2. Mechanism of the CRISPR/Cas9 gene editing system. The single guide RNA (sgRNA) directs the Cas9 nuclease to a
complementary genomic sequence, where Cas9 induces a double-strand break (DSB). The target sequence must be adjacent to a 5′-
NGG-3′ protospacer adjacent motif (PAM) for Cas9 activity. The DSB is repaired either by non-homologous end joining (NHEJ) or
homology-directed repair (HDR), the latter of which can utilize a DNA repair template to introduce precise genetic modifications or
exogenous sequences [25] .

approach in treating prostate cancer. Overall, suicide gene therapy holds promise for the treatment of
prostate cancer, and ongoing research aims to address the challenges and improve its efficacy [31-33] .

CELL THERAPY
Cell therapy uses immune cells like T cells to fight cancer. In prostate cancer, chimeric antigen receptor
(CAR) T cell therapy and dendritic cell vaccines have shown promise in early-phase clinical trials .
[34]
Chimeric antigen receptor T cell
This is one of the most advanced forms of cell therapy being explored for prostate cancer. This approach
involves genetically modifying a patient’s T cells (a type of immune cell) to express CARs - synthetic
receptors designed to recognize specific proteins on the surface of cancer cells. Once re-infused into the
[34]
patient, these CAR T cells can recognize and destroy prostate cancer cells . In prostate cancer, CAR T cell
therapy primarily targets the prostate-specific membrane antigen (PSMA), a protein highly expressed on the
surface of prostate cancer cells. By engineering T cells to target PSMA, researchers enhance the immune