SP94-Targeted Triblock Copolymer Nanoparticle Delivers Thymidine Kinase-p53-Nitroreductase Triple Therapeutic Gene and Restores Anticancer Function against Hepatocellular Carcinoma in Vivo

ACS Appl Mater Interfaces. 2020 Mar 11;12(10):11307-11319. doi: 10.1021/acsami.9b20071. Epub 2020 Mar 2.

Abstract

Gene-directed enzyme-prodrug therapy (GDEPT) is a promising approach for cancer therapy, but it suffers from poor targeted delivery in vivo. Polyethylenimine (PEI) is a cationic polymer efficient in delivering negatively charged nucleic acids across cell membranes; however, it is highly toxic in vivo. Hence, we efficiently reduced PEI toxicity without compromising its transfection efficiency by conjugating it with poly(d,l-lactic-co-glycolic acid) (PLGA) and poly(ethylene glycol) (PEG) as triblock copolymers through a multistep synthetic process. The synthesized nanoparticles showed efficient delivery of loaded nucleic acids to tumor cells in vitro and in vivo in mice. We used this nanoparticle to deliver a rationally engineered thymidine kinase (TK)-p53-nitroreductase (NTR) triple therapeutic gene against hepatocellular carcinoma (HCC), where p53 tumor suppressor gene is mutated in more than 85% of cancers. TK-p53-NTR triple gene therapy restores p53 function and potentiates cancer cell response to delivered prodrugs (ganciclovir (GCV) and CB1954). We used SP94 peptide-functionalized PLGA-PEG-PEI nanoparticles for the optimal delivery of TK-p53-NTR therapeutic gene in vivo. The nanoparticles prepared from the conjugated polymer showed high loading efficiency for the DNA and markedly enhanced TK-NTR-mediated gene therapy upon the simultaneous coexpression of p53 by the concurrent rescue of the endogenous apoptotic pathway in HCC cells of both p53-mutant and wild-type phenotypes in vitro. In vivo delivery of TK-p53-NTR genes by SP94-targeted PLGA-PEG-PEI NP in mice resulted in a strong expression of suicide genes selectively in tumors, and subsequent administration of GCV and CB1954 led to a decline in tumor growth, and established a superior therapeutic outcome against HCC. We demonstrate a highly efficient approach that exogenously supplements p53 to enable synergy with the outcome of TK-NTR suicide gene therapy against HCC.

Keywords: gene delivery; gene-directed enzyme−prodrug therapy (GDEPT); nitroreductase; p53; poly(lactic-co-glycolic acid); polyethylenimine; thymidine kinase.

MeSH terms

  • Animals
  • Antineoplastic Agents* / chemistry
  • Antineoplastic Agents* / metabolism
  • Antineoplastic Agents* / pharmacology
  • Carcinoma, Hepatocellular / metabolism*
  • Cell Line, Tumor
  • Female
  • Genetic Therapy / methods*
  • Liver Neoplasms / metabolism
  • Mice
  • Mice, Nude
  • Nanoparticles / chemistry*
  • Nitroreductases / genetics
  • Nitroreductases / metabolism
  • Polyesters / chemistry
  • Polyethylene Glycols / chemistry
  • Polyethyleneimine / chemistry*
  • Prodrugs / metabolism
  • Prodrugs / pharmacology
  • Thymidine Kinase / genetics
  • Thymidine Kinase / metabolism
  • Transfection
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Antineoplastic Agents
  • Polyesters
  • Prodrugs
  • Tumor Suppressor Protein p53
  • polyethylene glycol-poly(lactide-co-glycolide)
  • Polyethylene Glycols
  • Polyethyleneimine
  • Nitroreductases
  • Thymidine Kinase