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Modelling the Effects of Laser Photothermal Therapy on Proteins HSP70 and P53
Author(s) -
Milcarek Andrew,
Daus Kevin,
Alpaugh Mary,
Dobbins Tabbetha
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.775.6
Subject(s) - photothermal therapy , embryonic stem cell , hsp70 , extracellular , fibroblast , heat shock protein , biophysics , microbiology and biotechnology , cancer cell , cell type , cell , intracellular , chemistry , hek 293 cells , nanotechnology , in vitro , biochemistry , materials science , cancer , biology , gene , genetics
Gold nanoparticles (AuNPs) and nanorods (AuNRs) are able to conjoin with biological molecules and efficiently absorb light for conversion into heat energy. Thus, they are being investigated for treatment of a variety of cancers using lasers to induce the conversion to heat in a technique known as l aser ph oto t hermal t herapy (LPTT). Since its first demonstration in 2005, LPTT has been increasingly researched and its efficacy has been demonstrated in mouse models. However, details which focus on the effect of heat on surrounding healthy cells is extremely limited. Likewise, study of whether intracellular vs. extracellular AuNP and AuNR uptake is most beneficial (and for which cancer types) is not undertaken. In this research, we examine these two aspects of laser photothermal therapy with the research questions: (i) how does heat exposure regulate proteins within the surrounding cells, specifically HSP70 and P53 and (ii) how do the particles distribute themselves at the surface of and/or within the cell. Specific to objective (i), the proteins HSP70 and P53 are examined. HSP70 is a heat shock protein responsible for wound healing, particularly in thermal burns. P53 is the “tumor repair protein” which is responsible for regulating cell transcription. Assuring maintenance of normal concentrations and the correct conformation of these proteins in the surrounding healthy cells will be important for implementing LPTT in patient care. Specific to objective (ii), benign planar cell models, human embryonic kidney cells (HEK‐293) and primary mouse embryonic fibroblast cells (3T3), are studied with quantitative monitoring of particle uptake concentration and distribution on cell viability during the therapy treatment. Size, surface charge, and surface treatment determine whether particles will undergo cellular uptake. These and other protein additives (such as chitosan coatings) determine whether the particles will diffuse across the cell wall. Key to studying cellular uptake is the comparative examination of planar tumor HeLa cells and the 3D Mary‐X tumor cell model. Objective (ii) informs the LPTT community of researchers as to which AuNPs and AuNRs conditions enhance cellular uptake for tumor cells—without selective uptake in benign cells. Support or Funding Information The work is being carried out in Dr. Tabbetha Dobbins lab at Rowan University. Funding at this time provided by Rowan University Department of Biomedical and Translational Sciences.