DOI: 10.1002/asia.201300375

Aptamer-Conjugated Nanorods for Targeted Photothermal Therapy ofProstate Cancer Stem Cells

Jian Wang,[a, b] Kwame Sefah,[a] Meghan B. Altman,[a] Tao Chen,[a] Mingxu You,[a]

Zilong Zhao,[a] Cheng Zhi Huang,*[b] and Weihong Tan*[a]

Introduction

Prostate cancer is the second leading cause of cancer mor-tality in men in the Western world,[1] accounting for about30 000 deaths annually in the United States alone. It is esti-mated that 238 590 new cases and 29 720 deaths from pros-tate cancer will occur in the United States during 2013.[2]

About 97 % of patients are aged 50 and older, and about62 % are 65 years of age and older.[1] Since prostate canceris common in aging men, it is highly desirable to developmost effective therapeutic approaches with the fewest sideeffects. Currently, prostate cancer is generally diagnosed bya finding of elevated prostate-specific antigen (PSA) fol-lowed by a biopsy.[3] However, the major limitation of PSA

is the low specificity and high prevalence of detectingbenign prostatic hyperplasia, especially in older men.[4] Mostmen with prostate cancer benefit from hormone therapy inthe short term, such as androgen ablation therapy,[5] but, un-fortunately, few are cured, as the tumor eventually returns,which presumably results from the growth of cancer stemcells (CSCs).[6]

The CSC hypothesis was first proposed 50 years ago to ex-plain the observed functional heterogeneity within tumors.[7]

However, the first actual cancer stem cells were found inleukemia cells by Dick and colleagues in 1997.[8] This discov-ery revealed that a defined subset of cells was solely respon-sible for development of the disease. To date, CSCs havebeen observed in acute and chronic myeloid leukemia,[8] aswell as in various solid tumors, including those of the breast,brain, lung. and prostate gland.[9]

The function of normal stem cells in the adult organism isto renew and repair aged or damaged tissue, as a uniqueproliferative characteristic in each cell division.[10] Similarly,some tumor cells have the capacity of infinite self-renewalto drive tumor cell proliferation. As Scheme 1 A shows,these infinitely self-renewing tumor cells, termed cancerstem cells, represent only a small population of cells withina given tumor mass, but they have the potential to developdisease.[11] Otherwise, the bulk of tumor mass is composedof more differentiated cells that lack such self-renewal ca-pacity and are subject to apoptosis during tumor growth.[10]

In addition to their self-renewal property, CSCs appear tobe relatively resistant to commonly used cancer therapies,such as radiation and chemotherapy.[12] Thus, despite thesmall quantity of CSCs resident in the tumor mass, they maycause recurrence of the tumor many years after treatment.

Abstract: Prostate cancer results inabout 30 000 deaths annually in theUnited States, making it the secondleading cause of cancer mortality inmen in the Western world. Therefore,it is of great significance to capture andkill prostate cancer cells. It is wellknown that cancer stem cells are re-sponsible for the maintenance andmetastasis of tumors. This conceptoffers the possibility of developing a se-lective therapeutic approach in which

cancer stem cells are directly targetedand killed. In this work, aptamers se-lected against DU145 prostate cancercells (aptamer CSC1) and their subpo-pulation of cancer stem cells (aptamerCSC13) were linked to the surfaces ofgold nanorods (AuNRs), and the re-

sulting conjugates were successfullyused to target and kill both cancer cellsand cancer stem cells by near-infrared(NIR) laser irradiation. Even thoughcancer stem cells represent onlya small population among all cancercells, the entire cell viability was verylow after laser irradiation, suggestingthat tumorigenesis could be successful-ly controlled by this aptamer-basedmethod, thus paving the way for earlydiagnosis and targeted therapy.

Keywords: aptamers · cancer ·gold · nanostructures · photo-thermal therapy

[a] Dr. J. Wang, Dr. K. Sefah, Dr. M. B. Altman, T. Chen, Dr. M. You,Dr. Z. Zhao, Prof. W. TanCenter for Research at Bio/Nano InterfaceDepartment of ChemistryDepartment of Physiology and Functional GenomicsShands Cancer CenterUF Genetics InstituteMcKnight Brain InstituteUniversity of Florida, Gainesville, Florida 32611 (United States)Fax: (+1) 352-846-2410E-mail : Tan@chem.ufl.edu

[b] Dr. J. Wang, Prof. C. Z. HuangEducation Ministry Key Laboratory on Luminescence and Real-TimeAnalysisCollege of Pharmaceutical SciencesSouthwest University, Chongqing 400715, (P.R. China)Fax: (+86) 23-68367257E-mail : chengzhi@swu.edu.cn

Supporting information for this article is available on the WWWunder http://dx.doi.org/10.1002/asia.201300375.

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FULL PAPER

Current therapies, including surgery, radiotherapy, and che-motherapy, aim to eradicate or kill every cancer cell.[13] TheCSCs concept, however, suggests a fundamentally differentapproach because each tumor contains a small fraction ofstem cells responsible for the maintenance and propagationof the disease.[14] The development of new therapies thatspecifically target and kill CSCs may therefore provide lesstoxic and more long-lasting methods to kill the entiretumor.

The metastatic prostate cancer cell line DU145 is a modelof a particularly pernicious prostate cancer, which is hor-mone-insensitive and does not express PSA on the sur-face,[15] making it difficult to target by standard antigen–anti-body biorecognition strategies. Aptamers comprise a promis-ing class of targeting molecules.[16] Aptamers are single-stranded DNA or RNA molecules that have been evolvedin a test tube to bind to a specific target and offer many ad-vantages over the more commonly used targeting moietiessuch as antibodies.[17] As such, aptamers have been exten-sively used in drug delivery and cancer therapy.[16a, 18] For ex-

ample, aptamer–gold nanorod (AuNR) conjugates, whichshow excellent longitudinal plasmon resonance absorptionin the near-infrared (NIR) range and can efficiently transferNIR light to localized heating, have been used for photo-thermal therapy for leukemia.[18]

Our laboratory has selected several aptamers that recog-nize different subsets of DU145 cells through a SELEX(systematic evolution of ligands by exponential enrichment)process.[19] One aptamer, designated CSC1, recognizes allDU145 cells, while another, designated CSC13, recognizesonly prostate cancer stem cells. In this work, the DU145 cellline was used as a model to study selective photothermaltherapy for CSCs using aptamer–AuNRs conjugates asprobes. By covalent linkage of aptamers with AuNRs, bothspecific cell targeting and selective photothermal destructionof cancer cells can be achieved. The therapeutic resultshowed that AuNRs, as hyperthermia reagents, could selec-tively kill prostate cancer cells, including cancer stem cells,by virtue of the high specificity of aptamers. Since CSC13recognizes only prostate cancer stem cells, it showed high ef-ficacy in killing them, thus limiting the self-renewal poten-tial of CSCs and supplying, in turn, a broad-spectrum ap-proach to the targeting and killing of prostate cancer.

Results and Discussion

Characterization of Aptamer–AuNR Conjugates

In this work, aptamers were conjugated to AuNR surfacesthrough thiol–Au covalent linkages. The thiol-modified ap-tamers are composed of four important parts: 1) a thiolalkane linking the aptamers to the gold surface by formationof thiol–Au covalent bonds; 2) a hydrophilic 36 unit poly(-ethylene glycol) (PEG) as a linker to separate the alkanethiol from the aptamer so that signal quenching by the goldsurfaces can be avoided; 3) an aptamer segment to specifi-cally bind target cells; and 4) 3’-biotin with dye-labeledstreptavidin used as the signal reporter of aptamer to dem-onstrate the specific binding of aptamer with target cancercells.

Transmission electron microscopy (TEM) imaging ofAuNRs showed that the nanorods have an average width of13 nm and an average length of 45 nm, resulting in two reso-nance absorption bands at 516 nm and 780 nm, respectively.In order to reduce AuNR cytotoxicity and aggregation,thiol-terminated methoxypoly(ethylene glycol) (mPEG-SH)was introduced to coat the surface of AuNRs.[20] The absorp-tion spectra revealed that the absorptions bands changedvery little after modification with aptamers (Figure 1), sug-gesting the successful functionalization of AuNRs with apta-mer and mPEG-SH.

Aptamer Specifically Targets DU145 Cells

As shown in Scheme 1 B, aptamer CSC1 recognizes all pros-tate cancer cells, while aptamer CSC13 binds only a portionof the cells, that is, the prostate cancer stem cells. After co-

Abstract in Chinese:

Scheme 1. (A) Stem cell model of cancer self-renewal.[11] (B) Photother-mal therapy for prostate cancer using aptamer–NR conjugates.

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valent functionalization with AuNRs, the aptamer–AuNRconjugates proved to be highly promising for cell-specifictargeting with enhanced signaling, as well as increased bind-ing affinity.[20] In addition, the conjugates could be used fortargeted hyperthermia therapy. According to the CSC con-cept, CSC1–AuNRs were expected to kill all cancer cells,while CSC13–AuNRs would kill only CSCs. However, bothaptamer conjugates were demonstrated to induce the apop-tosis of prostate cancer cells because of the killing of cancerstem cells.

The specific binding of the aptamers and aptamer–AuNRconjugates was demonstrated by flow cytometric analysis(Figure 2). A random DNA library (Lib) and Lib–NR con-jugates showed only very weak fluorescence signals in flow

cytometry, thus suggesting that random sequences wereunable to specifically bind cancer cells. Aptamer CSC13, bycontrast, resulted in a strong fluorescence signal, thereby in-dicating a higher binding affinity of CSC13 to DU145 cellsas compared to Lib. Since CSCs comprise only a portion ofprostate cancer cells, CSC1, which binds the larger popula-tion of prostate cancer cells, led to a stronger signal thanCSC13.

Compared to individual aptamers, aptamer–AuNR conju-gates showed a >6-fold enhancement in fluorescence inten-sity owing to the presence of multiple aptamers on the goldsurface.[20] The results obtained after conjugation with NRsindicate that the aptamer probes maintained their bindingcapability and that the conjugates have an enhanced binding

affinity in cancer cell recognition. However, no significantenhancement in fluorescence intensity was detected forRamos cells, a control cell line which does not bind witheither CSC1 or CSC13 aptamers, further confirming the spe-cific recognition of the target cells by the aptamer–NR con-jugates.

Confocal microscopy also showed the specific binding ofthe aptamer to prostate cancer cells (Figure 3). After incu-bation with DU145 cells, aptamers emitted greater fluores-

cence on the cell surface compared with Lib because oftheir specific biorecognition of the membrane protein ofcancer cells. In addition, aptamer CSC1 showed a strongerred fluorescence than aptamer CSC13, indicating that moreCSC1 aptamer bound to the prostate cancer cells. However,an even more intense red fluorescence could be observedwhen aptamers were linked onto the gold surface, supplyingan enhanced fluorescence signal for imaging and significant-ly improving the binding affinity with cancer cells.[20] By con-trast, even though the Lib sequences was modified with goldnanorods, the fluorescence was too weak to detect by confo-cal imaging, suggesting the selective binding of aptamersCSC1 and CSC13 to target cancer cells.

Unconjugated AuNRs are Nontoxic to Cells

Some concern has been raised that free cetyltrimethylam-monium bromide (CTAB) used in the preparation ofCTAB-capped nanorods can be cytotoxic;[21] such nonspecif-ic toxicity would be unwelcome. In this work, AuNRs wereprepared using CTAB as a soft template.[22] To reduce thecytotoxicity of CTAB in the solution, centrifugation was per-formed twice to remove excess CTAB before and afterDNA-SH loading, respectively. Furthermore, the polymer ofmPEG-SH was introduced to stabilize the solution and min-imize the cytotoxicity.[21b] To check the cytotoxicity of theprobes, we added different concentrations of AuNRs to cellsalone, without the application of laser irradiation, and anMTS assay was performed on the cell solution. At a lowconcentration of AuNRs, the cell viability assay (Figure S1

Figure 1. Absorption spectra and TEM image of Au NRs. Concentra-tions: AuNRs, 0.8 nm ; aptamer, 200 nm. Scale bar: 50 nm.

Figure 2. Flow cytometric assay to monitor the specific binding of aptam-ers with a) DU145 cells (target cells) and b) Ramos cells (control cells).

Figure 3. Confocal microscopic images of DU145 cells after incubationwith aptamer and aptamer–NR conjugates and PI dye. In each picture,the left side is the fluorescence image (lexc =535 nm, lem =617 nm, O-5725 filter set), and the right side is the overlay of optical and fluores-cence images. Scale bars: 50 mm.

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in the Supporting Information) showed a low percentage ofdead cells. When the concentration of AuNRs reached thenanomolar level after enrichment by centrifugation, the cellviability was more than 84 % for both DU145 and Ramoscells, respectively, supporting the notion that the AuNRsthemselves are of low toxicity to the cells.

Photothermal Activation of AuNRs

AuNRs are especially attractive candidates for photothermaltherapy based on their facile synthesis with tunable absorp-tion and high absorption cross-section in the NIR region.[23]

These photonic properties can convert the absorbed photonenergy into thermal energy to induce cellular hyperthermiafor cells in close proximity, providing an opportunity for theclinical application of highly efficient and tumor-specificphotothermal therapy.[23, 24] We tested the hyperthermiaeffect by measuring the temperature as a function of time inreal time (Figure 4). For 0.4 nm AuNRs, the temperaturesharply increased from 25 8C to 55 8C because AuNRs ab-sorbed sufficient energy to generate heat.[25] The tempera-

ture of CSC1–AuNRs and CSC13–AuNRs increased from37 8C to 50 8C and 47 8C after binding to the DU145 cellline, respectively. The final temperature was slightly lowerbecause of the removal of unbound NRs. However, after in-cubation with control Ramos cells and removal of unboundaptamer–AuNRs, the temperatures were as low as those ofthe cells only, suggesting no binding of aptamer–AuNR con-jugates with the Ramos cell line, thus avoiding the harmfuleffects of the NIR laser. Therefore, the proposed aptamer–AuNRs supply a selective photothermal therapy for prostatecancer.

Aptamer–AuNRs Specifically Kill Cancer Cells

Confocal imaging (Figure 5) and MTS assay (Figure 6) wereused to monitor the therapeutic results after NIR laser irra-diation. The confocal imaging of cells was performed imme-diately after exposure to the NIR laser and staining with

propidium iodide (PI), an intercalating agent and a fluores-cent molecule that can be used as a stain to identify deadcells in a population.[18] Figure 5 demonstrates that thedirect irradiation of cells by the NIR laser maintaineda high cell viability due to the low light absorption of natu-ral endogenous cytochromes of cells in the NIR region.[26]

However, after incubation with aptamer–AuNR conjugatesand irradiation by the NIR laser, prostate cancer cellsshowed strong PI red fluorescence, thus suggesting thedeath of cancer cells by photothermal therapy.

The photothermal properties can be attributed to thelight–heat conversion mechanism, whereby AuNRs absorband convert laser light in the NIR range into heat. This heatis released to the immediate surrounding medium, increas-ing the surrounding temperature and resulting in the de-struction of adjacent cells. A previous investigation by ourgroup showed that the destructive effect was exerted bymeans of heat stress on the cells, rather than by mechanicalperforation of their membranes.[18] To confirm the specifickilling of target cancer cells, Ramos cells were used as a con-trol. Under conditions identical to those with the prostate

Figure 4. Temperature–time curves of aptamer–NR conjugates followingincubation with DU145 or Ramos cells upon laser irradiation. Laserwavelength, 812 nm.

Figure 5. Confocal microscopic images of DU145 and Ramos cells with-out and with incubation of aptamer–NR conjugates after irradiation witha NIR laser (812 nm). Cells were irradiated with NIR light at 600 mWfor 10 min and then stained with PI dye. In each picture, the left side isthe fluorescence image, and the right side is the overlay of optical andfluorescence images. Scale bars: 50 mm.

Figure 6. Cell viability data of cells incubated with aptamer–NR conju-gates and irradiated by an NIR laser (812 nm) for 10 min. P values werecalculated by the Student�s t-test: *p<0.05, **p<0.001, n =3.

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cancer cells, Ramos cells showed no PI signal. Thus, the re-sults indicate that the aptamer–AuNRs conjugates possessa high binding specificity and are, therefore, highly promis-ing for selective cell recognition and targeted cancer celltherapy.

MTS assays (Figure 6) of cancer cells were performedafter 10 minutes of NIR treatment, followed by incubationat 37 8C for two days. The data are expressed as the mean �standard deviation, and the statistical differences were as-sessed by the Student�s t-test. After NIR laser irradiation(812 nm) with CSC1- and CSC13-modified AuNRs, the cellviability decreased to 36 % (p<0.001) and 47 % (p<0.05),respectively, by the photothermal killing of cancer cells. Im-portantly, in confocal imaging (Figure 5), the red fluores-cence of DU145 cells incubated with CSC13–AuNRs wasmuch weaker than seen with CSC1–AuNRs. The CSC13–AuNRs conjugates bound and killed only a small subset ofCSCs, resulting in a correspondingly weaker PI signal. Here,MTS assay showed an approximate therapeutic result be-tween CSC1–AuNRs and CSC13–AuNRs conjugates basedon the killing of stem cells, which apparently could not self-renew two days after photothermal treatment, thereby indi-cating that the tumor could be controlled by the targetingand killing of CSCs. The control cell assay showed that theaptamer–AuNR conjugates were not as phototoxic (cell via-bility is more than 91 %) to the nontarget Ramos cells, illus-trating the selective photothermal therapy of aptamer–NRconjugates based on the stem cell therapy concept. AfterNIR laser treatment, both CSC1–NRs and CSC13–NRscould effectively kill cancer cells. Even though cancer stemcells account for a small fraction of the cancer cell popula-tion, the tumor can be controlled by targeting and killingthe cancer stem cells because of the loss of the self-renewalability of the entire tumor, thus leading to its apoptosis.

Conclusions

In this work, the metastatic prostate cancer cell line DU145was used as a model to study the cancer stem cell therapyconcept. DU145 cells are hormone-insensitive and do notexpress PSA, making this cell line an excellent model forhard-to-treat prostate cancers. To specifically target DU145cells, especially the stem cell fraction, we selected aptamersspecific for these cells and attached these aptamers toAuNRs. Incubation of cells with these conjugates followedby NIR laser treatment caused photothermal destruction ofcancer cells. In addition, the high specificity of aptamer–AuNR conjugates allowed the selective destruction of thecancer cells by NIR irradiation, thus avoiding harmful expo-sure of the surrounding normal tissue and, in turn, supplyingpromising candidates for use in phototherapy modalities.Importantly, the therapeutic effect suggested that the cancerstem cell concept can be used as a basis for effective andsafe applications in early diagnosis and targeted therapy. Itis fully anticipated that aptamer-based cancer stem cell ther-apy will be used to treat more types of intractable cancers.

Experimental Section

DNA Synthesis and Purification

The following aptamers[19] were selected for prostate cancer: CSC1 wasselected for all cancer cells, including cancer stem cells: 5’-ACC TTGGCT GTC GTG TTG TAG GTG GTT TGC TGC GGT GGG CTCAAG AAG AAA GCG CAA AGG TCA GTG GTC AGA GCG T-3’;CSC13 was selected for prostate cancer stem cells: 5’-ACC TTG GCTGTC GTG TTG TGG GGT GTC GTA TCT TTC GTG TCT TAT TATTTT CTA GGT GGA GGT CAG TGG TCA GAG CGT-3’; a random li-brary (Lib) was used as a negative control: 5’-CAG AGT GAC GCAGCA NNN NNN NNN NNN NNN NNN NNN NNN NNN NNN NNNNNN NNN NNN NNT GGA CAC GGT GGC TTA GT-3’, where N rep-resents A, T, C, or G.

All DNA oligomers were synthesized on an ABI3400 DNA/RNA synthe-sizer (Applied Biosystems, Foster City, CA) with 5’-thiol modificationand 3’-biotin controlled pore glass. Upon completion of synthesis, all olig-omers were deprotected in AMA (ammonium hydroxide/40% aqueousmethylamine 1:1) at 65 8C for 20–30 min, followed by mixing with 250 mL3.0m NaCl and 6.0 mL EtOH in 15 mL plastic tubes. After freezing at�20 8C, the samples were centrifuged at 4000 rpm at 4 8C for 20 min.Then, the precipitated DNA products were dissolved in 400 mL 0.2m trie-thylamine acetate (TEAA, Glen Research Corp.) for purification by re-verse-phase HPLC (ProStar, Varian, Walnut Creek, CA) on a C-18column, using a gradient mobile phase mixture of acetonitrile and aque-ous 0.1m triethylammonium amine (TEAA). The collected DNA prod-ucts were dried and detritylated in 200 mL 80 % acetic acid for 20 minand then precipitated with 20 mL 3.0 m NaCl and 500 mL ethanol, anddried by using a vacuum dryer. Finally, the absorbance at 260 nm wasmeasured with a Cary Bio-300 UV spectrometer (Varian, Walnut Creek,CA) to quantify DNA oligomers.

Preparation of AuNRs

AuNRs were prepared according to the seed-mediated protocol usingCTAB as a soft template.[22] First, in the presence of 7.5 � 10�2

m CTABsolution, gold seeds were prepared by reducing 2.5� 10�4

m HAuCl4·4H2Owith 9.0� 10�4

m ice-cold NaBH4. During vigorous stirring, the mixturerapidly developed a light brown color, and the mixture was then kept at25 8C until further use. A 25.0 mL growth solution was prepared contain-ing HAuCl4·4H2O (4.0 � 10�4

m) and CTAB (9.5 � 10�2m), followed by the

addition of 0.15 mL 0.01 m AgNO3 and 0.16 mL 0.1 ml-ascorbic acid (l-AA). During mixing, the solution immediately became colorless. Finally,0.11 mL of a 2 h-aged gold seed solution was added to the above solutionand stirred vigorously for 20 s with the color gradually becoming red.The mixed solution was left undisturbed overnight for further growth.

Preparation of Aptamer-Functionalized AuNRs

The functionalization of AuNRs with thiol-modified aptamers followeda published procedure.[20] Before conjugation, the thiol-functionalized ap-tamers (0.1 mm) were deprotected by 0.1 mm tris(2-carboxyethyl)phos-phine (TCEP) in 50 mm Tris-HCl (pH 7.5) buffer for 1 h at room temper-ature. The as-prepared AuNR solution (10.0 mL) was centrifuged twiceat 13 000 � g for 20 min to remove excess CTAB in the suspension, allow-ing the precipitate to be redispersed in water for further use. To stabilizeAuNRs and minimize their toxicity, 200 mL of fresh-prepared 2.0 mm

thiol-terminated methoxy poly(ethylene glycol) (mPEG-SH, Mw 5000)was used to coat the AuNRs (10.0 mL). The resulting AuNRs mixturewas left undisturbed for 1 h at room temperature, followed by the addi-tion of deprotected thiol-aptamer, incubation for 16 h, and aging for an-other 12 h in 0.1m NaCl. Finally, aptamer–AuNRs conjugates were puri-fied twice by centrifugation at 12 000 rpm for 5 min.

Cytotoxicity Assay

The cell viability of different cell lines was determined using the CellTit-er 96 AQueous One Solution Cell Proliferation Assay (MTS, Promega,Madison, WI, USA). Cells (2 � 105 cells per well) were first incubatedwith aptamer–AuNRs conjugates at 4 8C for 30 min and then washedwith washing buffer. After irradiation with a NIR laser (812 nm) for

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10 min, DU145 and Ramos cells were incubated in DMEM and RPMI1640 culture medium, respectively, at 37 8C under 5 % CO2 atmospherefor an additional 48 h. To measure the cytotoxicity, 120 mL MTS reagent(diluted 6 � with medium) were added to each well and incubated for 2 h.The absorbance was recorded at 490 nm using a Tecan Safire microplatereader.

Acknowledgements

We are grateful to Dr. Kathryn R. Williams for editing the manuscriptand John W. Munson for detecting the temperature curve with a lasersensor. Dr. J. Wang received financial support from the China Scholar-ship Council (CSC) and Southwest University (SWU112092). We ac-knowledge funding from U.S. NIH grants, the China NSFC (20805038),and the National Basic Research Program of China (2007CB935603,2010CB732402), as well as the China National Grand Program on KeyInfectious Disease (2009ZX10004-312) for partial support. We also re-ceived financial support from the Key Project of the Natural ScienceFoundation of China (90606003 and 21035005), the International Science& Technology Cooperation Program of China (2010DFB30300), as wellas the Hunan Provincial Natural Science Foundation of China(10JJ7002).

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Received: March 20, 2013Revised: April 20, 2013

Published online: && &&, 0000

Chem. Asian J. 2013, 00, 0 – 0 � 2013 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim6&&

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FULL PAPER

Photothermal Therapy

Jian Wang, Kwame Sefah,Meghan B. Altman, Tao Chen,Mingxu You, Zilong Zhao, ChengZhi Huang,* Weihong Tan* &&&&—&&&&

Aptamer-Conjugated Nanorods forTargeted Photothermal Therapy ofProstate Cancer Stem Cells

A more apt method : Aptamers CSC1and CSC-13 previously selected againstcancer cells and their subpopulation ofcancer stem cells (CSCs), respectively,were attached to the surface of goldnanorods (NRs) to target and kill pros-tate cancer cells (DU145 cell line) byphotothermal therapy. Although CSCsrepresent only a small populationamong all cancer cells, the whole cellviability was very low after laser irradi-ation, suggesting that tumorigenesiscould be successfully controlled by thisaptamer-based method.

Chem. Asian J. 2013, 00, 0 – 0 � 2013 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim7 &&

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