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Exosome-liposome hybrid nanoparticle codelivery of TP and miR497 conspicuously overcomes chemoresistant ovarian cancer

Li, Longxia, He, Di, Guo, Qianqian, Zhang, Zhiyoung, Ru, Dan, Wang, Liting, Gong, Ke, Liu, Fangfang, Duan, Yourong, Li, He·2022·Journal of Nanobiotechnology
DOI 10.1186/s12951-022-01264-5PMC PMC8787930
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Abstract

Background: Although cisplatin-based chemotherapy has been used as the first-line treatment for ovarian cancer (OC), tumor cells develop resistance to cisplatin during treatment, causing poor prognosis in OC patients. Studies have demonstrated that overactivation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is involved in tumor chemoresistance and that overexpression of microRNA-497 (miR497) may overcome OC chemotherapy resistance by inhibiting the mTOR pathway. However, the low transcriptional efficiency and unstable chemical properties of miR497 limit its clinical application. Additionally, triptolide (TP) was confirmed to possess a superior killing effect on cisplatin-resistant cell lines, partially through inhibiting the mTOR pathway. Even so, the clinical applications of TP are restricted by serious systemic toxicity and weak water solubility. Results: Herein, whether the combined application of miR497 and TP could further overcome OC chemoresistance by synergically suppressing the mTOR signaling pathway was investigated. Bioinspired hybrid nanoparticles formed by the fusion of CD47-expressing tumor exosomes and cRGD-modified liposomes (miR497/TP-HENPs) were prepared to codeliver miR497 and TP. In vitro results indicated that the nanoparticles were efficiently taken up by tumor cells, thus significantly enhancing tumor cell apoptosis. Similarly, the hybrid nanoparticles were effectively enriched in the tumor areas and exerted significant anticancer activity without any negative effects in vivo. Mechanistically, they promoted dephosphorylation of the overactivated PI3K/AKT/mTOR signaling pathway, boosted reactive oxygen species (ROS) generation and upregulated the polarization of macrophages from M2 to M1 macrophages. Conclusion: Overall, our findings may provide a translational strategy to overcome cisplatin-resistant OC and offer a potential solution for the treatment of other cisplatin-resistant tumors. Graphical Abstract:

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Fig. 1 Diagram of the formative process and mechanism of action of miR497/TP-HENPs. miR497/TP-HENPs were synthesized by membrane fusion and biomineralization methods. First, liposomes were synthesized by assembly with DSPE-PEG1k-cRGD, phosphatidylcholine (PC), cholesterol and encapsulated TP. Then, liposomes and exosomes were fused by membrane fusion. Finally, CaP adsorbed miR497 on the surface of nanoparticles. The mechanisms by which miR497/TP-HENPs operated in OC cells were as follows: a the enhanced permeability and retention (EPR) effect were generated from the nanoscale size of the nanoplatforms, b the homing targeting of exosomes and cRGD further enhanced the targeting efficiency of nanoparticles, c CD47 on the exosome surface avoided nanoparticle clearance by the MPS system, d miR497 and TP synergistically inhibited the PI3K/AKT/mTOR pathway, e TP stimulated ROS production, and f TP modulated polarization of M2 macrophages into M1 macrophages, synergistically overcoming OC resistance
Fig. 1 Diagram of the formative process and mechanism of action of miR497/TP-HENPs. miR497/TP-HENPs were synthesized by membrane fusion and biomineralization methods. First, liposomes were synthesized by assembly with DSPE-PEG1k-cRGD, phosphatidylcholine (PC), cholesterol and encapsulated TP. Then, liposomes and exosomes were fused by membrane fusion. Finally, CaP adsorbed miR497 on the surface of nanoparticles. The mechanisms by which miR497/TP-HENPs operated in OC cells were as follows: a the enhanced permeability and retention (EPR) effect were generated from the nanoscale size of the nanoplatforms, b the homing targeting of exosomes and cRGD further enhanced the targeting efficiency of nanoparticles, c CD47 on the exosome surface avoided nanoparticle clearance by the MPS system, d miR497 and TP synergistically inhibited the PI3K/AKT/mTOR pathway, e TP stimulated ROS production, and f TP modulated polarization of M2 macrophages into M1 macrophages, synergistically overcoming OC resistanceCC BY · PubMed Central
Fig. 2 Synthesis and characterization of HENPs. A Representative image of exosomes captured by TEM at different magnifications. B The size distribution of exosomes and C the particle size distribution range of exosomes were measured by NTA. D Morphology of HENPs detected by TEM. E Size distribution of liposomes and HENPs. F The FRET assay showed the successful fusion of exosomes and liposomes. G Protein expression of exosomes and HENPs nanovesicles. H and I The nanoparticle size and PDI over a period of time were used to assess the stability of nanoparticles. J Zeta potential distribution of exosomes, liposomes and HENPs. K and L Release profiles of miRNC and TP at pH values of 5.5 and 7.4 at 37 °C
Fig. 2 Synthesis and characterization of HENPs. A Representative image of exosomes captured by TEM at different magnifications. B The size distribution of exosomes and C the particle size distribution range of exosomes were measured by NTA. D Morphology of HENPs detected by TEM. E Size distribution of liposomes and HENPs. F The FRET assay showed the successful fusion of exosomes and liposomes. G Protein expression of exosomes and HENPs nanovesicles. H and I The nanoparticle size and PDI over a period of time were used to assess the stability of nanoparticles. J Zeta potential distribution of exosomes, liposomes and HENPs. K and L Release profiles of miRNC and TP at pH values of 5.5 and 7.4 at 37 °CCC BY · PubMed Central
Fig. 3 Cellular uptake of HENPs in vitro. CLSM was used to observe the cellular uptake of free RB or different nanoparticles encapsulated with RB in A SKOV3-CDDP and B SKOV3 cells (at a scale of 50 µm). C, D FCM was performed to analyze the cellular uptake of HENPs in SKOV3-CDDP and SKOV3 cells at 4 h. E, F RB HENPs cellular uptake mechanism determined by blocker. The data are expressed as the mean ± SD (ns: p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001)
Fig. 3 Cellular uptake of HENPs in vitro. CLSM was used to observe the cellular uptake of free RB or different nanoparticles encapsulated with RB in A SKOV3-CDDP and B SKOV3 cells (at a scale of 50 µm). C, D FCM was performed to analyze the cellular uptake of HENPs in SKOV3-CDDP and SKOV3 cells at 4 h. E, F RB HENPs cellular uptake mechanism determined by blocker. The data are expressed as the mean ± SD (ns: p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001)CC BY · PubMed Central
Fig. 4 The combination of miR497and TP overcomes chemotherapy resistance in OC in vitro. A Images of the positive cells with calcein-AM staining. B Apoptotic SKOV3-CDDP and SKOV3 cells were analyzed by FCM after 48 h of treatment with different drugs in vitro. C, D Quantitative percentages of apoptotic cells in two ovarian cancer cell lines. E Western blotting images showed the expression levels of proteins of the PI3K/AKT/mTOR signaling pathway. The data are expressed as the mean ± SD (ns: p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001)
Fig. 4 The combination of miR497and TP overcomes chemotherapy resistance in OC in vitro. A Images of the positive cells with calcein-AM staining. B Apoptotic SKOV3-CDDP and SKOV3 cells were analyzed by FCM after 48 h of treatment with different drugs in vitro. C, D Quantitative percentages of apoptotic cells in two ovarian cancer cell lines. E Western blotting images showed the expression levels of proteins of the PI3K/AKT/mTOR signaling pathway. The data are expressed as the mean ± SD (ns: p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001)CC BY · PubMed Central
Fig. 5 miR497/TP-HENPs boost intracellular ROS and induce M2 to M1 polarization of macrophages. A ROS in SKOV3-CDDP cells. Scale bar: 50 μm. B Quantitative analysis of ROS in SKOV3-CDDP cells by FCM. C Analysis of the expression of HIF-α using WB assay. D GSH quantity in SKOV3-CDDP cells. E, F Cell supernatant levels of TNF-α and TGF-β1 in different treatment groups of RAW264.7 macrophages. G, H FCM analysis of the expression of M1 macrophage markers (F4/80 + CD86 +) and quantitative analysis of the MFI of PE-CD86. I The ratio of M1/M2 subtype macrophages treated with different groups in vitro
Fig. 5 miR497/TP-HENPs boost intracellular ROS and induce M2 to M1 polarization of macrophages. A ROS in SKOV3-CDDP cells. Scale bar: 50 μm. B Quantitative analysis of ROS in SKOV3-CDDP cells by FCM. C Analysis of the expression of HIF-α using WB assay. D GSH quantity in SKOV3-CDDP cells. E, F Cell supernatant levels of TNF-α and TGF-β1 in different treatment groups of RAW264.7 macrophages. G, H FCM analysis of the expression of M1 macrophage markers (F4/80 + CD86 +) and quantitative analysis of the MFI of PE-CD86. I The ratio of M1/M2 subtype macrophages treated with different groups in vitroCC BY · PubMed Central
Fig. 6 The targeting and antitumor activity of miR497/TP-HENPs in vivo. A In vivo imaging to observe the tumor targeting ability of different nanoparticles. B Ex vivo fluorescence images of the main organs and tumors isolated from mice bearing subcutaneous SKOV3-CDDP tumors. C Quantitative analysis of Dir distribution in the tumor site postinjection elevated by the fluorescence intensity measured in (A). D Quantitative assessment of the mean fluorescence intensity in major organs and isolated subcutaneous tumors. E Representative photographs of subcutaneous tumors harvested from all treatment groups. F Growth record curves of subcutaneous tumors in nude mice during the experiment. G The inhibition rate of OC treated with various drugs. H The H&E staining and TUNEL staining. I Immunohistochemical detection of ki67, p-PI3K, p-AKT, and p-mTOR. Scare bar: 100 µm
Fig. 6 The targeting and antitumor activity of miR497/TP-HENPs in vivo. A In vivo imaging to observe the tumor targeting ability of different nanoparticles. B Ex vivo fluorescence images of the main organs and tumors isolated from mice bearing subcutaneous SKOV3-CDDP tumors. C Quantitative analysis of Dir distribution in the tumor site postinjection elevated by the fluorescence intensity measured in (A). D Quantitative assessment of the mean fluorescence intensity in major organs and isolated subcutaneous tumors. E Representative photographs of subcutaneous tumors harvested from all treatment groups. F Growth record curves of subcutaneous tumors in nude mice during the experiment. G The inhibition rate of OC treated with various drugs. H The H&E staining and TUNEL staining. I Immunohistochemical detection of ki67, p-PI3K, p-AKT, and p-mTOR. Scare bar: 100 µmCC BY · PubMed Central
Fig. 7 miR497/TP-HENPs induced ROS production in cisplatin-resistant OC and regulated macrophage polarization from M2 to M1 in vivo. A The ROS of tumor sections after treatments. Scale bar: 50 µm. B, C Serum levels of TNF-α and TGF-β1 in different treatment groups in vivo. One-way ANOVA was used to determine significant differences; *p < 0.05; **p < 0.01, ***p < 0.001, compared with the indicated groups. D Immunofluorescence staining images of different macrophage markers (M1, F4/80 + CD86 + and M2, F4/80 + CD206 +) in tumor tissue sections. Scale bar: 50 µm
Fig. 7 miR497/TP-HENPs induced ROS production in cisplatin-resistant OC and regulated macrophage polarization from M2 to M1 in vivo. A The ROS of tumor sections after treatments. Scale bar: 50 µm. B, C Serum levels of TNF-α and TGF-β1 in different treatment groups in vivo. One-way ANOVA was used to determine significant differences; *p < 0.05; **p < 0.01, ***p < 0.001, compared with the indicated groups. D Immunofluorescence staining images of different macrophage markers (M1, F4/80 + CD86 + and M2, F4/80 + CD206 +) in tumor tissue sections. Scale bar: 50 µmCC BY · PubMed Central
Fig. 8 In vivo safety assessment. A Body weight change curves of nude mice in all treatment groups during the trial. B-F Changes in biochemical indicators of liver and kidney function in mice after the last injection. All data were from three replicates. G H&E staining of the main organs of nude mice and the structural damage sites were noted with black arrows. Scale bar: 100 μm
Fig. 8 In vivo safety assessment. A Body weight change curves of nude mice in all treatment groups during the trial. B-F Changes in biochemical indicators of liver and kidney function in mice after the last injection. All data were from three replicates. G H&E staining of the main organs of nude mice and the structural damage sites were noted with black arrows. Scale bar: 100 μmCC BY · PubMed Central

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Cites

Research works printed but not linked: 57

  1. Siegel RL, Miller KD, Fuchs HE, Jemal A. Cancer Statistics, 2021. CA Cancer J Clin. 2021;71:7–33. · DOI · Paper page
  2. Yang J, Huang S, Cheng S, Jin Y, Zhang N, Wang Y. Application of ovarian cancer organoids in precision medicine: key challenges and current opportunities. Front Cell Dev Biol. 2021;9:701429.2.
  3. Lheureux S, Braunstein M, Oza AM. Epithelial ovarian cancer: evolution of management in the era of precision medicine. CA Cancer J Clin. 2019;69:280–304. · DOI
  4. Wang Y, Qiao X, Yang X, Yuan M, Xian S, Zhang L, Yang D, Liu S, Dai F, Tan Z, Cheng Y. The role of a drug-loaded poly (lactic co-glycolic acid) (PLGA) copolymer stent in the treatment of ovarian cancer. Cancer Biol Med. 2020;17:237–50. · DOI
  5. Spears N, Lopes F, Stefansdottir A, Rossi V, De Felici M, Anderson RA, Klinger FG. Ovarian damage from chemotherapy and current approaches to its protection. Hum Reprod Update. 2019;25:673–93. · DOI
  6. Mukherjee A, Huynh V, Gaines K, Reh WA, Vasquez KM. Targeting the high-mobility group box 3 protein sensitizes chemoresistant ovarian cancer cells to cisplatin. Cancer Res. 2019;79:3185–91. · DOI
  7. Tong L, Zhao Q, Datan E, Lin GQ, Minn I, Pomper MG, Yu B, Romo D, He QL, Liu JO. Triptolide: reflections on two decades of research and prospects for the future. Nat Prod Rep. 2021;38:843–60. · DOI
  8. Noel P, Von Hoff DD, Saluja AK, Velagapudi M, Borazanci E, Han H. Triptolide and its derivatives as cancer therapies. Trends Pharmacol Sci. 2019;40:327–41. · DOI · Paper page
  9. Hou ZY, Tong XP, Peng YB, Zhang BK, Yan M. Broad targeting of triptolide to resistance and sensitization for cancer therapy. Biomed Pharmacother. 2018;104:771–80. · DOI
  10. Gao J, Zhang Y, Liu X, Wu X, Huang L, Gao W. Triptolide: pharmacological spectrum, biosynthesis, chemical synthesis and derivatives. Theranostics. 2021;11:7199–221. · DOI
  11. Beglyarova N, Banina E, Zhou Y, Mukhamadeeva R, Andrianov G, Bobrov E, Lysenko E, Skobeleva N, Gabitova L, Restifo D, et al. Screening of conditionally reprogrammed patient-derived carcinoma cells identifies ERCC3-MYC interactions as a target in pancreatic cancer. Clin Cancer Res. 2016;22:6153–63. · DOI
  12. Wei J, Yan Y, Chen X, Qian L, Zeng S, Li Z, Dai S, Gong Z, Xu Z. The roles of plant-derived triptolide on non-small cell lung cancer. Oncol Res. 2019;27:849–58. · DOI
  13. Zhu J, Wang H, Chen F, Lv H, Xu Z, Fu J, Hou Y, Xu Y, Pi J. Triptolide enhances chemotherapeutic efficacy of antitumor drugs in non-small-cell lung cancer cells by inhibiting Nrf2-ARE activity. Toxicol Appl Pharmacol. 2018;358:1–9. · DOI
  14. Wang R, Ma X, Su S, Liu Y. Triptolide antagonized the cisplatin resistance in human ovarian cancer cell line A2780/CP70 via hsa-mir-6751. Future Med Chem. 2018;10:1947–55. · DOI
  15. Huang G, Hu H, Zhang Y, Zhu Y, Liu J, Tan B, Chen T. Triptolide sensitizes cisplatin-resistant human epithelial ovarian cancer by inhibiting the phosphorylation of AKT. J Cancer. 2019;10:3012–20. · DOI
  16. Ho JN, Byun SS, Lee S, Oh JJ, Hong SK, Lee SE, Yeon JS. Synergistic antitumor effect of triptolide and cisplatin in cisplatin resistant human bladder cancer cells. J Urol. 2015;193:1016–22. · DOI
  17. Chen YW, Lin GJ, Chuang YP, Chia WT, Hueng DY, Lin CK, Nieh S, Sytwu HK. Triptolide circumvents drug-resistant effect and enhances 5-fluorouracil antitumor effect on KB cells. Anticancer Drugs. 2010;21:502–13. · DOI
  18. Burris HA 3rd. Overcoming acquired resistance to anticancer therapy: focus on the PI3K/AKT/mTOR pathway. Cancer Chemother Pharmacol. 2013;71:829–42. · DOI
  19. Huang Y, Wu S, Zhang Y, Wang L, Guo Y. Antitumor effect of triptolide in T-cell lymphoblastic lymphoma by inhibiting cell viability, invasion, and epithelial-mesenchymal transition via regulating the PI3K/AKT/mTOR pathway. Onco Targets Ther. 2018;11:769–79. · DOI
  20. Kim SH, Kang JG, Kim CS, Ihm SH, Choi MG, Yoo HJ, Lee SJ. Synergistic cytotoxicity of BIIB021 with triptolide through suppression of PI3K/Akt/mTOR and NF-κB signal pathways in thyroid carcinoma cells. Biomed Pharmacother. 2016;83:22–32. · DOI
  21. Brozovic A, Majhen D, Roje V, Mikac N, Jakopec S, Fritz G, Osmak M, Ambriovic-Ristov A. alpha(v)beta(3) Integrin-mediated drug resistance in human laryngeal carcinoma cells is caused by glutathione-dependent elimination of drug-induced reactive oxidative species. Mol Pharmacol. 2008;74:298–306. · DOI
  22. Brozovic A, Ambriović-Ristov A, Osmak M. The relationship between cisplatin-induced reactive oxygen species, glutathione, and BCL-2 and resistance to cisplatin. Crit Rev Toxicol. 2010;40:347–59. · DOI
  23. Zhong YY, Chen HP, Tan BZ, Yu HH, Huang XS. Triptolide avoids cisplatin resistance and induces apoptosis via the reactive oxygen species/nuclear factor-κB pathway in SKOV3(PT) platinum-resistant human ovarian cancer cells. Oncol Lett. 2013;6:1084–92. · DOI
  24. Jiang X, Cao G, Gao G, Wang W, Zhao J, Gao C. Triptolide decreases tumor-associated macrophages infiltration and M2 polarization to remodel colon cancer immune microenvironment via inhibiting tumor-derived CXCL12. J Cell Physiol. 2021;236:193–204. · DOI
  25. Zheng Y, Zhang WJ, Wang XM. Triptolide with potential medicinal value for diseases of the central nervous system. CNS Neurosci Ther. 2013;19:76–82. · DOI
  26. Xi C, Peng S, Wu Z, Zhou Q, Zhou J. Toxicity of triptolide and the molecular mechanisms involved. Biomed Pharmacother. 2017;90:531–41. · DOI
  27. Wang S, Xu J, Guo Y, Cai Y, Ren X, Zhu W, Geng M, Meng L, Jiang C, Lu S. MicroRNA-497 reduction and increase of its family member microRNA-424 lead to dysregulation of multiple inflammation related genes in synovial fibroblasts with rheumatoid arthritis. Front Immunol. 2021;12: 619392.
  28. Nigita G, Distefano R, Veneziano D, Romano G, Rahman M, Wang K, Pass H, Croce CM, Acunzo M, Nana-Sinkam P. Tissue and exosomal miRNA editing in non-small cell lung cancer. Sci Rep. 2018;8:10222. · DOI
  29. Zhang T, Feng X, Zhou T, Zhou N, Shi X, Zhu X, Qiu J, Deng G, Qiu C. miR-497 induces apoptosis by the IRAK2/NF-κB axis in the canine mammary tumour. Vet Comp Oncol. 2021;19:69–78. · DOI
  30. Gui ZL, Wu TL, Zhao GC, Lin ZX, Xu HG. MicroRNA-497 suppress osteosarcoma by targeting MAPK/Erk pathway. Bratisl Lek Listy. 2017;118:449–52.
  31. Wang L, Ji XB, Wang LH, Qiu JG, Zhou FM, Liu WJ, Wan DD, Lin MC, Liu LZ, Zhang JY, Jiang BH. Regulation of microRNA-497-targeting AKT2 influences tumor growth and chemoresistance to cisplatin in lung cancer. Front Cell Dev Biol. 2020;8:840. · DOI
  32. Shao XJ, Miao MH, Xue J, Xue J, Ji XQ, Zhu H. The down-regulation of microRNA-497 contributes to cell growth and cisplatin resistance through PI3K/Akt pathway in osteosarcoma. Cell Physiol Biochem. 2015;36:2051–62. · DOI
  33. Xu S, Fu GB, Tao Z, OuYang J, Kong F, Jiang BH, Wan X, Chen K. MiR-497 decreases cisplatin resistance in ovarian cancer cells by targeting mTOR/P70S6K1. Oncotarget. 2015;6:26457–71. · DOI
  34. Chen X, Liang H, Zhang J, Zen K, Zhang CY. Secreted microRNAs: a new form of intercellular communication. Trends Cell Biol. 2012;22:125–32. · DOI · Paper page
  35. Guan W, Xu DW, Ji CH, Wang CN, Liu Y, Tang WQ, Gu JH, Chen YM, Huang J, Liu JF, Jiang B. Hippocampal miR-206–3p participates in the pathogenesis of depression via regulating the expression of BDNF. Pharmacol Res. 2021;174: 105932. · DOI
  36. Zhang L, Jing D, Wang L, Sun Y, Li JJ, Hill B, Yang F, Li Y, Lam KS. Unique photochemo-immuno-nanoplatform against orthotopic xenograft oral cancer and metastatic syngeneic breast cancer. Nano Lett. 2018;18:7092–103. · DOI
  37. Zhai Y, Ran W, Su J, Lang T, Meng J, Wang G, Zhang P, Li Y. Traceable bioinspired nanoparticle for the treatment of metastatic breast cancer via NIR-trigged intracellular delivery of methylene blue and cisplatin. Adv Mater. 2018. https://doi.org/10.1002/adma.201802378. · DOI
  38. Sailor MJ, Park JH. Hybrid nanoparticles for detection and treatment of cancer. Adv Mater. 2012;24:3779–802. · DOI
  39. Wang Y, Zhang Z, Zheng C, Zhao X, Zheng Y, Liu Q, Liu Y, Shi L. Multistage adaptive nanoparticle overcomes biological barriers for effective chemotherapy. Small. 2021;17: e2100578.
  40. Wang G, Zannikou M, Lofchy L, Li Y, Gaikwad H, Balyasnikova IV, Simberg D. Liposomal extravasation and accumulation in tumors as studied by fluorescence microscopy and imaging depend on the fluorescent label. ACS Nano. 2021. https://doi.org/10.1021/acsnano.1c02982. · DOI
  41. Song Y, Guo X, Fu J, He B, Wang X, Dai W, Zhang H, Zhang Q. Dual-targeting nanovesicles enhance specificity to dynamic tumor cells in vitro and in vivo via manipulation of αvβ3-ligand binding. Acta Pharm Sin B. 2020;10:2183–97. · DOI
  42. Gu Y, Lai S, Dong Y, Fu H, Song L, Chen T, Duan Y, Zhang Z. AZD9291 resistance reversal activity of a ph-sensitive nanocarrier dual-loaded with chloroquine and FGFR1 inhibitor in NSCLC. Adv Sci (Weinh). 2021;8:2002922. · DOI
  43. Cohen O, Betzer O, Elmaliach-Pnini N, Motiei M, Sadan T, Cohen-Berkman M, Dagan O, Popovtzer A, Yosepovich A, Barhom H, et al. “Golden” exosomes as delivery vehicles to target tumors and overcome intratumoral barriers: in vivo tracking in a model for head and neck cancer. Biomater Sci. 2021;9:2103–14. · DOI
  44. Pan S, Zhang Y, Huang M, Deng Z, Zhang A, Pei L, Wang L, Zhao W, Ma L, Zhang Q, Cui D. Urinary exosomes-based engineered nanovectors for homologously targeted chemo-chemodynamic prostate cancer therapy via abrogating EGFR/AKT/NF-kB/IkB signaling. Biomaterials. 2021;275: 120946.
  45. Wang C, Steinmetz NF. CD47 Blockade and Cowpea Mosaic Virus Nanoparticle In Situ Vaccination Triggers Phagocytosis and Tumor Killing. Adv Healthc Mater. 2019;8: e1801288.
  46. Lv Q, Cheng L, Lu Y, Zhang X, Wang Y, Deng J, Zhou J, Liu B, Liu J. Thermosensitive exosome-liposome hybrid nanoparticle-mediated chemoimmunotherapy for improved treatment of metastatic peritoneal cancer. Adv Sci (Weinh). 2020;7:2000515. · DOI
  47. Cheng L, Zhang X, Tang J, Lv Q, Liu J. Gene-engineered exosomes-thermosensitive liposomes hybrid nanovesicles by the blockade of CD47 signal for combined photothermal therapy and cancer immunotherapy. Biomaterials. 2021;275: 120964. · DOI
  48. Piffoux M, Silva AKA, Wilhelm C, Gazeau F, Tareste D. Modification of extracellular vesicles by fusion with liposomes for the design of personalized biogenic drug delivery systems. ACS Nano. 2018;12:6830–42. · DOI
  49. Yong T, Zhang X, Bie N, Zhang H, Zhang X, Li F, Hakeem A, Hu J, Gan L, Santos HA, Yang X. Tumor exosome-based nanoparticles are efficient drug carriers for chemotherapy. Nat Commun. 2019;10:3838. · DOI · Paper page
  50. He D, Xu X, Li L, Chen C, Gong K, Guo Q, Liu F, Wang Y, Duan Y, Li H. Functional exosome-mediated delivery of triptolide endowed with targeting properties as chemotherapy carriers for ovarian carcinoma. J Biomed Nanotechnol. 2021;17:426–38. · DOI
  51. Zhou BG, Wei CS, Zhang S, Zhang Z, Gao HM. Matrine reversed multidrug resistance of breast cancer MCF-7/ADR cells through PI3K/AKT signaling pathway. J Cell Biochem. 2018;119:3885–91. · DOI
  52. Musa F, Alard A, David-West G, Curtin JP, Blank SV, Schneider RJ. Dual mTORC1/2 inhibition as a novel strategy for the resensitization and treatment of platinum-resistant ovarian cancer. Mol Cancer Ther. 2016;15:1557–67. · DOI
  53. Zhang Y, Dong Y, Fu H, Huang H, Wu Z, Zhao M, Yang X, Guo Q, Duan Y, Sun Y. Multifunctional tumor-targeted PLGA nanoparticles delivering Pt(IV)/siBIRC5 for US/MRI imaging and overcoming ovarian cancer resistance. Biomaterials. 2021;269: 120478.
  54. Rudin CM, Yang Z, Schumaker LM, VanderWeele DJ, Newkirk K, Egorin MJ, Zuhowski EG, Cullen KJ. Inhibition of glutathione synthesis reverses Bcl-2-mediated cisplatin resistance. Cancer Res. 2003;63:312–8.
  55. Rodriguez-Garcia A, Lynn RC, Poussin M, Eiva MA, Shaw LC, O’Connor RS, Minutolo NG, Casado-Medrano V, Lopez G, Matsuyama T, Powell DJ Jr. CAR-T cell-mediated depletion of immunosuppressive tumor-associated macrophages promotes endogenous antitumor immunity and augments adoptive immunotherapy. Nat Commun. 2021;12:877. · DOI
  56. Wang H, Zheng Y, Sun Q, Zhang Z, Zhao M, Peng C, Shi S. Ginsenosides emerging as both bifunctional drugs and nanocarriers for enhanced antitumor therapies. J Nanobiotechnology. 2021;19:322. · DOI
  57. Ru D, Ding C, Liu L, Liu H, Shen M, Duan Y, Li H. pH sensitive triptolide-loaded liposome calcium phosphate nanoparticles exhibit enhanced anti-tumor activities against ovarian cancer without damaging the reproductive system. J Biomed Nanotechnol. 2017;13:1413–24. · DOI

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Metadata

Authors
Li, L., He, D., Guo, Q., Zhang, Z., Ru, D., Wang, L., Gong, K., Liu, F., Duan, Y., & Li, H.
Venue
Journal of Nanobiotechnology
Publisher
Springer Science and Business Media LLC
Published
2022-01-25
Volume
20
Issue
1
ISSN
1477-3155
DOI
10.1186/s12951-022-01264-5
PMC
PMC8787930
Cited by
206
References
3
Language
en
Licence
Funders
National Natural Science Foundation of China (81874479, 81773272, 81972886, 82174135)

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