Publication:
CXCR4-targeted nanoparticles reduce cell viability, induce apoptosis and inhibit SDF-1α induced BT-549-Luc cell migration in vitro

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Issued Date

2017

Resource Type

Article

File Type

application/pdf

ISSN

15672018

DOI

10.2174/1567201814666170216130448

Other identifier(s)

2-s2.0-85041060602

Rights Holder(s)

Scopus

Bibliographic Citation

Current Drug Delivery. Vol 14, No.8 (2017), p.1060-1070

Suggested Citation

Chittasupho C., Kewsuwan P., Murakami T. CXCR4-targeted nanoparticles reduce cell viability, induce apoptosis and inhibit SDF-1α induced BT-549-Luc cell migration in vitro. Current Drug Delivery. Vol 14, No.8 (2017), p.1060-1070. doi:10.2174/1567201814666170216130448 Retrieved from: https://hdl.handle.net/20.500.14740/4744

Title

CXCR4-targeted nanoparticles reduce cell viability, induce apoptosis and inhibit SDF-1α induced BT-549-Luc cell migration in vitro

Author(s)

Chittasupho C.
 Kewsuwan P.
 Murakami T.

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. Method: 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. Conclusion: 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. © 2017 Bentham Science Publishers.

Subject(s)

Chemokine
 Chemokine receptor CXCR4 antagonist
 Cytotoxic agent
 Doxorubicin
 Lfc 131
 Nanoparticle
 Polyglactin
 Stromal cell derived factor 1alpha
 Tyrosinylarginylarginine sodium iodide glycine
 Unclassified drug
 Antineoplastic antibiotic
 Chemokine receptor CXCR4
 CXCL12 protein, human
 CXCR4 protein, human
 Doxorubicin
 Lactic acid
 Ligand
 Nanoparticle
 Oligopeptide
 Polyglycolic acid
 Polylactic acid-polyglycolic acid copolymer
 Stromal cell derived factor 1
 Apoptosis
 Article
 Breast cancer cell line
 BT 549 Luc cell line
 Cancer chemotherapy
 Cell migration
 Cell viability
 Comparative study
 Controlled study
 Dose response
 Drug delivery system
 Drug efficacy
 Drug protein binding
 Human
 Human cell
 In vitro study
 Incubation time
 Internalization
 MTT assay
 Priority journal
 Antagonists and inhibitors
 Apoptosis
 Breast tumor
 Cell motion
 Cell proliferation
 Cell survival
 Chemistry
 Drug effect
 Drug screening
 Metabolism
 Pathology
 Tumor cell culture
 Antibiotics, Antineoplastic
 Apoptosis
 Breast Neoplasms
 Cell Movement
 Cell Proliferation
 Cell Survival
 Chemokine CXCL12
 Doxorubicin
 Drug Screening Assays, Antitumor
 Humans
 Lactic Acid
 Ligands
 Nanoparticles
 Oligopeptides
 Polyglycolic Acid
 Receptors, CXCR4
 Tumor Cells, Cultured

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URI

https://hdl.handle.net/20.500.14740/4744

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Scopus: Year 1983-2021

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