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Research Article

Inhibition of Wnt signaling by Frizzled7 antibody-coated nanoshells sensitizes triple-negative breast cancer cells to the autophagy regulator chloroquine

Jianxin Wang1, Megan N. Dang1, Emily S. Day1,2,3( )
Department of Biomedical Engineering, University of Delaware, Newark, DE 19716, USA
Department of Materials Science and Engineering, University of Delaware, Newark, DE 19716, USA
Helen F. Graham Cancer Center & Research Institute, Newark, DE 19713, USA
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Abstract

Despite improvements in our understanding of the biology behind triple-negative breast cancer (TNBC), it remains a devastating disease due to lack of an effective targeted therapy. Inhibiting Wnt signaling is a promising strategy to combat TNBC because Wnt signaling drives TNBC progression, chemoresistance, and stemness. However, Wnt inhibition can lead to upregulation of autophagy, which confers therapeutic resistance. This provides an opportunity for combination therapy, as autophagy inhibitors applied concurrently with Wnt inhibitors could increase treatment efficacy. Here, we applied the autophagy inhibitor chloroquine (CQ) to TNBC cells in combination with Frizzled7 antibody-coated nanoshells (FZD7-NS) that suppress Wnt signaling by blocking Wnt ligand/FZD7 receptor interactions, and evaluated this dual treatment in vitro. We found that FZD7-NS can inhibit Axin2 and CyclinD1, two targets of canonical Wnt signaling, and increase the expression of LC3, an autophagy marker. When FZD7-NS and CQ are applied together, they reduce the expression of several stemness genes in TNBC cells, leading to inhibition of TNBC cell migration and self-renewal. Notably, co-delivery of FZD7-NS and CQ is more effective than either therapy alone or the combination of CQ with free FZD7 antibodies. This demonstrates that the nanocarrier design is important to its therapeutic utility. Overall, these findings indicate that combined regulation of Wnt signaling and autophagy by FZD7-NS and CQ is a promising strategy to combat TNBC.

Keywords

nanomedicinenanoparticlescombination therapyantibody deliverycancer stem cells

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References

[1]
Anders, C. K.; Carey, L. A. Biology, metastatic patterns, and treatment of patients with triple-negative breast cancer. Clin. Breast Cancer 2009, 9, S73-S81.
Crossref Google Scholar
[2]
Dent, R.; Hanna, W. M.; Trudeau, M.; Rawlinson, E.; Sun, P.; Narod, S. A. Pattern of metastatic spread in triple-negative breast cancer. Breast Cancer Res. Treat .2009, 115, 423-428.
Crossref Google Scholar
[3]
Pohl, S. G.; Brook, N.; Agostino, M.; Arfuso, F.; Kumar, A. P.; Dharmarajan, A. Wnt signaling in triple-negative breast cancer. Oncogenesis 2017, 6, e310.
Crossref Google Scholar
[4]
Dey, N.; Barwick, B. G.; Moreno, C. S.; Ordanic-Kodani, M.; Chen, Z. J.; Oprea-Ilies, G.; Tang, W. N.; Catzavelos, C.; Kerstann, K. F.; Sledge, G. W. et al. Wnt signaling in triple negative breast cancer is associated with metastasis. BMC Cancer 2013, 13, 537.
Crossref Google Scholar
[5]
King, T. D.; Suto, M. J.; Li, Y. H. The Wnt/β-catenin signaling pathway: A potential therapeutic target in the treatment of triple negative breast cancer. J. Cell. Biochem .2012, 113, 13-18.
Crossref Google Scholar
[6]
Yang, L.; Wu, X.; Wang, Y.; Zhang, K.; Wu, J.; Yuan, Y. C.; Deng, X.; Chen, L.; Kim, C. C. H.; Lau, S. et al. FZD7 has a critical role in cell proliferation in triple negative breast cancer. Oncogene 2011, 30, 4437-4446.
Crossref Google Scholar
[7]
Riley, R. S.; Day, E. S. Frizzled7 antibody-functionalized nanoshells enable multivalent binding for wnt signaling inhibition in triple negative breast cancer cells. Small 2017, 13, 1700544.
Crossref Google Scholar
[8]
Ma, B.; Hottiger, M. O. Crosstalk between Wnt/β-catenin and NF-κB signaling pathway during inflammation. Front. Immunol .2016, 7, 378.
Crossref Google Scholar
[9]
Morris, S. A. L.; Huang, S. Y. Crosstalk of the Wnt/β-catenin pathway with other pathways in cancer cells. Genes Dis .2016, 3, 41-47.
Crossref Google Scholar
[10]
Jeong, W. J.; Ro, E. J.; Choi, K. Y. Interaction between Wnt/ β-catenin and RAS-ERK pathways and an anti-cancer strategy via degradations of β-catenin and RAS by targeting the Wnt/β-catenin pathway. NPJ Precis. Oncol .2018, 2, 5.
Crossref Google Scholar
[11]
Nàger, M.; Sallán, M. C.; Visa, A.; Pushparaj, C.; Santacana, M.; Macià, A.; Yeramian, A.; Cantí, C.; Herreros, J. Inhibition of Wnt-CTNNB1 signaling upregulates SQSTM1 and sensitizes glioblastoma cells to autophagy blockers. Autophagy 2018, 14, 619-636.
Crossref Google Scholar
[12]
Petherick, K. J.; Williams, A. C.; Lane, J. D.; Ordóñez-Morán, P.; Huelsken, J.; Collard, T. J.; Smartt, H. J. M.; Batson, J.; Malik, K.; Paraskeva, C. et al. Autolysosomal β-catenin degradation regulates Wnt-autophagy-p62 crosstalk. EMBO J .2013, 32, 1903-1916.
Crossref Google Scholar
[13]
Turcios, L.; Chacon, E.; Garcia, C.; Eman, P.; Cornea, V.; Jiang, J. Y.; Spear, B.; Liu, C. M.; Watt, D. S.; Marti, F. et al. Autophagic flux modulation by Wnt/β-catenin pathway inhibition in hepatocellular carcinoma. PLoS One 2019, 14, e0212538.
Crossref Google Scholar
[14]
Fu, Y. J.; Chang, H.; Peng, X. L.; Bai, Q.; Yi, L.; Zhou, Y.; Zhu, J. D.; Mi, M. T. Resveratrol inhibits breast cancer stem-like cells and induces autophagy via suppressing Wnt/β-catenin signaling pathway. PLoS One 2014, 9, e102535.
Crossref Google Scholar
[15]
Su, N.; Wang, P. P.; Li, Y. Role of Wnt/β-catenin pathway in inducing autophagy and apoptosis in multiple myeloma cells. Oncol. Lett .2016, 12, 4623-4629.
Crossref Google Scholar
[16]
Ávalos, Y.; Canales, J.; Bravo-Sagua, R.; Criollo, A.; Lavandero, S; Quest, A. F. G. Tumor suppression and promotion by autophagy. BioMed Res. Int .2014, 2014, 603980.
Crossref Google Scholar
[17]
Chittaranjan, S.; Bortnik, S.; Dragowska, W. H.; Xu, J.; Abeysundara, N.; Leung, A.; Go, N. E.; DeVorkin, L.; Weppler, S. A.; Gelmon, K. et al. Autophagy inhibition augments the anticancer effects of epirubicin treatment in anthracycline-sensitive and -resistant triple-negative breast cancer. Clin. Cancer Res .2014, 20, 3159-3173.
Crossref Google Scholar
[18]
Rubinsztein, D. C.; Codogno, P.; Levine, B. Autophagy modulation as a potential therapeutic target for diverse diseases. Nat. Rev. Drug Discov .2012, 11, 709-730.
Crossref Google Scholar
[19]
Oldenburg, S. J.; Averitt, R. D.; Westcott, S. L.; Halas, N. J. Nanoengineering of optical resonances. Chem. Phys. Lett .1998, 288, 243-247.
Crossref Google Scholar
[20]
Melamed, J. R.; Ioele, S. A.; Hannum, A. J.; Ullman, V. M.; Day, E. S. Polyethylenimine-spherical nucleic acid nanoparticles against GLI1 reduce the chemoresistance and stemness of glioblastoma cells. Mol. Pharm .2018, 15, 5135-5145.
Crossref Google Scholar
[21]
Manders, E. M. M.; Verbeek, F. J.; Aten, J. A. Measurement of co-localization of objects in dual-colour confocal images. J. Microsc .1993, 169, 375-382.
Crossref Google Scholar
[22]
Stauffer, W.; Sheng, H. J.; Lim, H. N. EzColocalization: An ImageJ plugin for visualizing and measuring colocalization in cells and organisms. Sci. Rep .2018, 8, 15764.
Crossref Google Scholar
[23]
Wang, J. X.; Potocny, A. M.; Rosenthal, J.; Day, E. S. Gold nanoshell-linear tetrapyrrole conjugates for near infrared-activated dual photodynamic and photothermal therapies. ACS Omega 2020, 5, 926-940.
Crossref Google Scholar
[24]
Riley, R. S.; Melamed, J. R.; Day, E. S. Enzyme-linked immunosorbent assay to quantify targeting molecules on nanoparticles. In Targeted Drug Delivery: Methods and Protocols. Sirianni, R. W.; Behkam, B., Eds.; Humana Press: New York, NY, 2018; pp 145-157.
Crossref
[25]
de Puig, H.; Bosch, I.; Carré-Camps, M.; Hamad-Schifferli, K. Effect of the protein corona on antibody-antigen binding in nanoparticle sandwich immunoassays. Bioconjugate Chem .2017, 28, 230-238.
Crossref Google Scholar
[26]
Sahay, G.; Alakhova, D. Y.; Kabanov, A. V. Endocytosis of nanomedicines. J. Control. Release 2010, 145, 182-195.
Crossref Google Scholar
[27]
Oh, E.; Delehanty, J. B.; Sapsford, K. E.; Susumu, K.; Goswami, R.; Blanco-Canosa, J. B.; Dawson, P. E.; Granek, J.; Shoff, M.; Zhang, Q. et al. Cellular uptake and fate of PEGylated gold nanoparticles is dependent on both cell-penetration peptides and particle size. ACS Nano 2011, 5, 6434-6448.
Crossref Google Scholar
[28]
Chithrani, D. B. Intracellular uptake, transport, and processing of gold nanostructures. Mol. Membr. Biol .2010, 27, 299-311.
Crossref Google Scholar
[29]
Nativo, P.; Prior, I. A.; Brust, M. Uptake and intracellular fate of surface-modified gold nanoparticles. ACS Nano 2008, 2, 1639-1644.
Crossref Google Scholar
[30]
Wang, L. M.; Liu, Y.; Li, W.; Jiang, X. M.; Ji, Y. L.; Wu, X. C.; Xu, L. G.; Qiu, Y.; Zhao, K.; Wei, T. T. et al. Selective targeting of gold nanorods at the mitochondria of cancer cells: Implications for cancer therapy. Nano Lett .2011, 11, 772-780.
Crossref Google Scholar
[31]
Frantz, M. C.; Wipf, P. Mitochondria as a target in treatment. Environ. Mol. Mutagen .2010, 51, 462-475.
Crossref Google Scholar
[32]
Weinberg, S. E.; Chandel, N. S. Targeting mitochondria metabolism for cancer therapy. Nat. Chem. Biol .2015, 11, 9-15.
Crossref Google Scholar
[33]
Fulda, S.; Galluzzi, L.; Kroemer, G. Targeting mitochondria for cancer therapy. Nat. Rev. Drug Discov .2010, 9, 447-464.
Crossref Google Scholar
[34]
Murphy, M. P.; Hartley, R. C. Mitochondria as a therapeutic target for common pathologies. Nat. Rev. Drug Discov .2018, 17, 865-886.
Crossref Google Scholar
[35]
Pathak, R. K.; Kolishetti, N.; Dhar, S. Targeted nanoparticles in mitochondrial medicine. Wiley Interdiscip. Rev. Nanomed. Nanobiotechnol .2015, 7, 315-329.
Crossref Google Scholar
[36]
Marrache, S.; Pathak, R. K.; Dhar, S. Formulation and optimization of mitochondria-targeted polymeric nanoparticles. In Mitochondrial Medicine: Volume II, Manipulating Mitochondrial Function. Weissig, V.; Edeas, M., Eds.; Humana Press: New York, 2015; pp 103-112.
[37]
Picard, M.; Wallace, D. C.; Burelle, Y. The rise of mitochondria in medicine. Mitochondrion 2016, 30, 105-116.
Crossref Google Scholar
[38]
Gao, C.; Cao, W. P.; Bao, L.; Zuo, W.; Xie, G. M.; Cai, T. T.; Fu, W.; Zhang, J.; Wu, W.; Zhang, X. et al. Autophagy negatively regulates Wnt signalling by promoting Dishevelled degradation. Nat. Cell Biol .2010, 12, 781-790.
Crossref Google Scholar
[39]
Bilir, B.; Kucuk, O.; Moreno, C. S. Wnt signaling blockage inhibits cell proliferation and migration, and induces apoptosis in triple-negative breast cancer cells. J. Transl. Med .2013, 11, 280.
Crossref Google Scholar
[40]
Liu, C. G.; Sun, L. S.; Yang, J.; Liu, T.; Yang, Y. L.; Kim, S. M.; Ou, X. Y.; Wang, Y. N.; Sun, L.; Zaidi, M. et al. FSIP1 regulates autophagy in breast cancer. Proc. Natl. Acad. Sci. USA 2018, 115, 13075-13080.
Crossref Google Scholar
[41]
Reya, T.; Morrison, S. J.; Clarke, M. F.; Weissman, I. L. Stem cells, cancer, and cancer stem cells. Nature 2001, 414, 105-111.
Crossref Google Scholar
[42]
Reya, T.; Clevers, H. Wnt signalling in stem cells and cancer. Nature 2005, 434, 843-850.
Crossref Google Scholar
[43]
Pan, H. Z.; Cai, N.; Li, M.; Liu, G. H.; Izpisua Belmonte, J. C. Autophagic control of cell ‘stemness’. EMBO Mol. Med .2013, 5, 327-331.
Crossref Google Scholar
[44]
García-Prat, L.; Martínez-Vicente, M.; Perdiguero, E.; Ortet, L.; Rodríguez-Ubreva, J.; Rebollo, E.; Ruiz-Bonilla, V.; Gutarra, S.; Ballestar, E.; Serrano, A. L. et al. Autophagy maintains stemness by preventing senescence. Nature 2016, 529, 37-42.
Crossref Google Scholar
[45]
Desai, A.; Yan, Y.; Gerson, S. L. Concise reviews: Cancer stem cell targeted therapies: Toward clinical success. Stem Cells Transl. Med .2019, 8, 75-81.
Crossref Google Scholar
[46]
Saygin, C.; Matei, D.; Majeti, R.; Reizes, O.; Lathia, J. D. Targeting cancer stemness in the clinic: From hype to hope. Cell Stem Cell 2019, 24, 25-40.
Crossref Google Scholar
[47]
Yu, F.; Li, J.; Chen, H.; Fu, J.; Ray, S.; Huang, S.; Zheng, H.; Ai, W. Kruppel-like factor 4 (KLF4) is required for maintenance of breast cancer stem cells and for cell migration and invasion. Oncogene 2011, 30, 2161-2172.
Crossref Google Scholar
[48]
Nagata, T.; Shimada, Y.; Sekine, S.; Moriyama, M.; Hashimoto, I.; Matsui, K.; Okumura, T.; Hori, T.; Imura, J.; Tsukada, K. KLF4 and NANOG are prognostic biomarkers for triple-negative breast cancer. Breast Cancer 2017, 24, 326-335.
Crossref Google Scholar
[49]
Lu, X.; Mazur, S. J.; Lin, T.; Appella, E.; Xu, Y. The pluripotency factor Nanog promotes breast cancer tumorigenesis and metastasis. Oncogene 2014, 33, 2655-2664.
Crossref Google Scholar
[50]
Zhang, J. M.; Wei, K.; Jiang, M. OCT4 but not SOX2 expression correlates with worse prognosis in surgical patients with triple-negative breast cancer. Breast Cancer 2018, 25, 447-455.
Crossref Google Scholar
[51]
Cheng, C. C.; Shi, L. H.; Wang, X. J.; Wang, S. X.; Wan, X. Q.; Liu, S. R.; Wang, Y. F.; Lu, Z.; Wang, L. H.; Ding, Y. Stat3/Oct-4/c-Myc signal circuit for regulating stemness-mediated doxorubicin resistance of triple-negative breast cancer cells and inhibitory effects of WP1066. Int. J. Oncol .2018, 53, 339-348.
Crossref Google Scholar
[52]
Imrich, S.; Hachmeister, M.; Gires, O. EpCAM and its potential role in tumor-initiating cells. Cell Adh. Migr .2012, 6, 30-38.
Crossref Google Scholar
[53]
Osta, W. A.; Chen, Y.; Mikhitarian, K.; Mitas, M.; Salem, M.; Hannun, Y. A.; Cole, D. J.; Gillanders, W. E. EpCAM is overexpressed in breast cancer and is a potential target for breast cancer gene therapy. Cancer Res .2004, 64, 5818-5824.
Crossref Google Scholar
[54]
Lobba, A. R. M.; Forni, M. F.; Carreira, A. C. O.; Sogayar, M. C. Differential expression of CD90 and CD14 stem cell markers in malignant breast cancer cell lines. Cytometry A 2012, 81, 1084-1091.
Crossref Google Scholar
[55]
Lu, H. H.; Clauser, K. R.; Tam, W. L.; Fröse, J.; Ye, X.; Eaton, E. N.; Reinhardt, F.; Donnenberg, V. S.; Bhargava, R.; Carr, S. A. et al. A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages. Nat. Cell Biol .2014, 16, 1105-1117.
Crossref Google Scholar
[56]
Wheatley, S. P.; Altieri, D. C. Survivin at a glance. J. Cell Sci .2019, 132, jcs223826.
Crossref Google Scholar
[57]
Cho, Y. H.; Han, K. M.; Kim, D.; Lee, J.; Lee, S. H.; Choi, K. W.; Kim, J.; Han, Y. M. Autophagy regulates homeostasis of pluripotency-associated proteins in hESCs. Stem Cells 2014, 32, 424-435.
Crossref Google Scholar
[58]
Liu, C. C.; DeRoo, E. P.; Stecyk, C.; Wolsey, M.; Szuchnicki, M.; Hagos, E. G. Impaired autophagy in mouse embryonic fibroblasts null for Krüppel-like Factor 4 promotes DNA damage and increases apoptosis upon serum starvation. Mol. Cancer 2015, 14, 101.
Crossref Google Scholar
[59]
Hsieh, P. N.; Zhou, G. J.; Yuan, Y. Y.; Zhang, R. L.; Prosdocimo, D. A.; Sangwung, P.; Borton, A. H.; Boriushkin, E.; Hamik, A.; Fujioka, H. et al. A conserved KLF-autophagy pathway modulates nematode lifespan and mammalian age-associated vascular dysfunction. Nat. Commun .2017, 8, 914.
Crossref Google Scholar
[60]
Hasmim, M.; Janji, B.; Khaled, M.; Noman, M. Z.; Louache, F.; Bordereaux, D.; Abderamane, A.; Baud, V.; Mami-Chouaib, F.; Chouaib, S. Cutting edge: NANOG activates autophagy under hypoxic stress by binding to BNIP3L promoter. J. Immunol .2017, 198, 1423-1428.
Crossref Google Scholar
[61]
Liao, X. D.; Zhang, R. L.; Lu, Y.; Prosdocimo, D. A.; Sangwung, P.; Zhang, L. L.; Zhou, G. J.; Anand, P.; Lai, L.; Leone, T. C. et al. Kruppel-like factor 4 is critical for transcriptional control of cardiac mitochondrial homeostasis. J. Clin. Invest .2015, 125, 3461-3476.
Crossref Google Scholar
[62]
Kumar, A.; Bhanja, A.; Bhattacharyya, J.; Jaganathan, B. G. Multiple roles of CD90 in cancer. Tumor Biol .2016, 37, 11611-11622.
Crossref Google Scholar
[63]
van der Gun, B. T. F.; Melchers, L. J.; Ruiters, M. H. J.; de Leij, L. F. M. H.; McLaughlin, P. M. J.; Rots, M. G. EpCAM in carcinogenesis: The good, the bad or the ugly. Carcinogenesis 2010, 31, 1913-1921.
Crossref Google Scholar
[64]
Garg, H.; Suri, P.; Gupta, J. C.; Talwar, G. P.; Dubey, S. Survivin: A unique target for tumor therapy. Cancer Cell Int .2016, 16, 49.
Crossref Google Scholar
[65]
Siddharth, S.; Das, S.; Nayak, A.; Kundu, C. N. SURVIVIN as a marker for quiescent-breast cancer stem cells—An intermediate, adherent, pre-requisite phase of breast cancer metastasis. Clin. Exp. Meta .2016, 33, 661-675.
Crossref Google Scholar
[66]
Levy, J. M. M.; Towers, C. G.; Thorburn, A. Targeting autophagy in cancer. Nat. Rev. Cancer 2017, 17, 528-542.
Crossref Google Scholar
[67]
Lefort, S.; Joffre, C.; Kieffer, Y.; Givel, A. M.; Bourachot, B.; Zago, G.; Bieche, I.; Dubois, T.; Meseure, D.; Vincent-Salomon, A. et al. Inhibition of autophagy as a new means of improving chemotherapy efficiency in high-LC3B triple-negative breast cancers. Autophagy 2014, 10, 2122-2142.
Crossref Google Scholar
[68]
O’Reilly, E. A.; Gubbins, L.; Sharma, S.; Tully, R.; Guang, M. H. Z.; Weiner-Gorzel, K.; McCaffrey, J.; Harrison, M.; Furlong, F.; Kell, M. et al. The fate of chemoresistance in triple negative breast cancer (TNBC). BBA Clin .2015, 3, 257-275.
Crossref Google Scholar
[69]
Pérez-Hernández, M.; Arias, A.; Martínez-García, D.; Pérez-Tomás, R.; Quesada, R.; Soto-Cerrato, V. Targeting autophagy for cancer treatment and tumor chemosensitization. Cancers 2019, 11, 1599.
Crossref Google Scholar
[70]
Pelt, J.; Busatto, S.; Ferrari, M.; Thompson, E. A.; Mody, K.; Wolfram, J. Chloroquine and nanoparticle drug delivery: A promising combination. Pharmacol. Ther .2018, 191, 43-49.
Crossref Google Scholar
[71]
Abdullah, L. N.; Chow, E. K. H. Mechanisms of chemoresistance in cancer stem cells. Clin. Transl. Med .2013, 2, 3.
Crossref Google Scholar
[72]
Zhou, Z.; Feng, Z. W.; Hu, D.; Yang, P.; Gur, M.; Bahar, I.; Cristofanilli, M.; Gradishar, W. J.; Xie, X. Q.; Wan, Y. A novel small-molecule antagonizes PRMT5-mediated KLF4 methylation for targeted therapy. EBioMedicine 2019, 44, 98-111.
Crossref Google Scholar
[73]
Choi, D. S.; Blanco, E.; Kim, Y. S.; Rodriguez, A. A.; Zhao, H.; Huang, T. H. M.; Chen, C. L.; Jin, G. X.; Landis, M. D.; Burey, L. A. et al. Chloroquine eliminates cancer stem cells through deregulation of Jak2 and DNMT1. STEM CELLS 2014, 32, 2309-2323.
Crossref Google Scholar
[74]
Bouchard, G.; Therriault, H.; Geha, S.; Bérubé-Lauzière, Y.; Bujold, R.; Saucier, C.; Paquette, B. Stimulation of triple negative breast cancer cell migration and metastases formation is prevented by chloroquine in a pre-irradiated mouse model. BMC Cancer 2016, 16, 361.
Crossref Google Scholar
[75]
Liang, D. H.; Choi, D. S.; Ensor, J. E.; Kaipparettu, B. A.; Bass, B. L.; Chang, J. C. The autophagy inhibitor chloroquine targets cancer stem cells in triple negative breast cancer by inducing mitochondrial damage and impairing DNA break repair. Cancer Lett .2016, 376, 249-258.
Crossref Google Scholar
Nano Research
Volume 13 Issue 6,
June 2020
Pages 1693-1703
DOI: 10.1007/s12274-020-2795-8
Cite this article:
Wang J, Dang MN, Day ES. Inhibition of Wnt signaling by Frizzled7 antibody-coated nanoshells sensitizes triple-negative breast cancer cells to the autophagy regulator chloroquine. Nano Research, 2020, 13(6): 1693-1703. https://doi.org/10.1007/s12274-020-2795-8
Topics:
Antibodies Cell death DiseasesNanoshells Nanostructured materialsSignaling

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Received: 03 March 2020
Revised: 01 April 2020
Accepted: 06 April 2020
Published: 25 April 2020
© Tsinghua University Press and Springer-Verlag GmbH Germany, part of Springer Nature 2020
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