title: CXCR4-targeted Nanoparticles Reduce Cell Viability, Induce Apoptosis and Inhibit SDF-1α Induced BT-549-Luc Cell Migration In Vitro.
abstract: BACKGROUND
  CXCR4 possesses a critical role in several intracellular events such as chemotaxis, invasion and adhesion, which are associated with metastasis of cancer cell.
  
  
  OBJECTIVE
  In this study, CXCR4 targeted polymeric nanoparticle was developed for delivering cytotoxic drug and blocking the chemokine induced migration of cells expressing CXCR4.
  
  
  METHODS
  A peptide which was a linear form of CXCR4 antagonist (LFC131) was attached to PLGA nanoparticles (LFC131-NPs) and PLGA nanoparticles encapsulating DOX (LFC131-DOX-NPs). The cellular binding and internalization of LFC131-DOX-NPs were investigated.
  
  
  RESULTS
  The binding and internalization of LFC131-DOX-NPs were higher and more rapidly compared to unconjugated NPs. LFC131-NPs blocked SDF-1α induced migration of BT-549-Luc cells. MTT assays demonstrated that LFC131-NPs and LFC131-DOX-NPs decreased cell viability in a dose dependent manner in 24, 72 and 120 h incubation.
  
  
  CONCLUSIONS
  A treatment concept of blocking breast cancer cell migration from interaction with SDF- 1α by using LFC131-NPs and then attacking breast cancer cells with doxorubicin might increase the efficacy of current breast cancer treatment.
authors.affiliation: Department of Pharmaceutical Technology, Faculty of Pharmacy, Srinakharinwirot University, Ongkarak, Nakhonnayok, 26120. Thailand.
authors.forename: Chuda
authors.initials: C
authors.lastname: Chittasupho
authors.affiliation: Thailand Institute of Nuclear Technology, Ongkarak, Nakhonnayok, 26120. Thailand.
authors.forename: Prartana
authors.initials: P
authors.lastname: Kewsuwan
authors.affiliation: Department of Microbiology, Saitama Medical University, Iruma-gun, Saitama 350-0495. Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Murakami
mesh_terms: D000903:Antibiotics, Antineoplastic / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000188:drug therapy / Q000473:pathology*; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D054377:Chemokine CXCL12 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D004317:Doxorubicin / Q000008:administration & dosage* / Q000737:chemistry / Q000494:pharmacology; D004354:Drug Screening Assays, Antitumor; D006801:Humans; D019344:Lactic Acid / Q000737:chemistry; D008024:Ligands; D053758:Nanoparticles / Q000008:administration & dosage*; D009842:Oligopeptides / Q000737:chemistry; D011100:Polyglycolic Acid / Q000737:chemistry; D000077182:Polylactic Acid-Polyglycolic Acid Copolymer; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000903:Antibiotics, Antineoplastic; C515255:CXCL12 protein, human; C527276:CXCR4 protein, human; D054377:Chemokine CXCL12; D008024:Ligands; D009842:Oligopeptides; D019718:Receptors, CXCR4; D000077182:Polylactic Acid-Polyglycolic Acid Copolymer; D011100:Polyglycolic Acid; D019344:Lactic Acid; D004317:Doxorubicin
keywords: Breast cancer; CXCR4; LFC131; PLGA; metastasis; nanoparticle