pH-Sensitive Shell-Core Platform Block DNA Repair Pathway To Amplify Irreversible DNA Damage of Triple Negative Breast Cancer

ACS Appl Mater Interfaces. 2019 Oct 23;11(42):38417-38428. doi: 10.1021/acsami.9b12140. Epub 2019 Oct 10.

Abstract

Triple negative breast cancer (TNBC) is insensitive to either chemotherapy or endocrine therapy because of the powerful DNA reparation and the negative expression of surface antigens, which urgently claims for an effective approach to improve the prognosis. Herein, DNA repair blocker BRCA1 small interfering RNA (siRNA) was introduced with cisplatin (Pt) into the elaborately designed pH-sensitive shell-core platform to enhance the chemotherapeutic treatment effect by silencing the DNA repair related gene. In this platform, BRCA1 siRNA and Pt prodrug (Pro-Pt) were separately encapsulated in the porous outer shell and hydrophobic inner core with extremely high encapsulation efficiency and stability effectively preventing them from degradation during circulation. Suitable size and urokinase plasminogen activator analogues (uPA) with high affinity for the uPA receptor (uPAR) realized an excellent dual passive and active tumor targeting ability. Moreover, the exposed PEG hydrophilic chain prevented the nanoparticles (NPs) from precipitating by serum protein or inactivating by nuclease in the blood cycle. Most importantly, the degradable CaP (calcium ions and phosphate ions) shell with smart pH sensitivity would dissipate from NPs in the lysosomes to burst the lysosome membranes so as to guarantee the lysosomal escape and the sequential release of the siRNA and Pro-Pt where the BRCA1 siRNA blocked the DNA repairing pathway followed by reducing Pro-Pt to Pt for irreversible DNA damage. Hence, the uPA-SP@CaP NPs provided a promising strategy for high-efficiency treatment of TNBC along with bringing new hope for more patients.

Keywords: irreversible DNA damage; lysosomal escape; pH-sensitive sequential release; synergistic treatment; triple negative breast cancer.

MeSH terms

  • Animals
  • BRCA1 Protein / antagonists & inhibitors
  • BRCA1 Protein / genetics
  • BRCA1 Protein / metabolism*
  • Calcium / chemistry
  • Cell Line, Tumor
  • Cisplatin / chemistry
  • Cisplatin / pharmacology
  • DNA Damage / drug effects*
  • Female
  • Humans
  • Hydrogen-Ion Concentration
  • Hydrophobic and Hydrophilic Interactions
  • Mice
  • Mice, Inbred BALB C
  • Nanoparticles / chemistry*
  • Phosphates / chemistry
  • Porosity
  • Prodrugs / chemistry
  • Prodrugs / pharmacology*
  • Prodrugs / therapeutic use
  • RNA, Small Interfering / chemistry
  • RNA, Small Interfering / metabolism*
  • Receptors, Urokinase Plasminogen Activator / genetics
  • Receptors, Urokinase Plasminogen Activator / metabolism
  • Triple Negative Breast Neoplasms / drug therapy
  • Triple Negative Breast Neoplasms / metabolism
  • Triple Negative Breast Neoplasms / pathology
  • Urokinase-Type Plasminogen Activator / chemistry
  • Urokinase-Type Plasminogen Activator / metabolism

Substances

  • BRCA1 Protein
  • BRCA1 protein, human
  • Phosphates
  • Prodrugs
  • RNA, Small Interfering
  • Receptors, Urokinase Plasminogen Activator
  • Urokinase-Type Plasminogen Activator
  • Cisplatin
  • Calcium