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Folic acid-conjugated mesoporous silica particles as nanocarriers of natural prodrugs for cancer targeting and antioxidant action

AbouAitah, Khaled, Swiderska-Sroda, Anna, Farghali, Ahmed A., Wojnarowicz, Jacek, Stefanek, Agata, Gierlotka, Stanislaw, Opalinska, Agnieszka, Allayeh, Abdou K., Ciach, Tomasz, Lojkowski, Witold·2018·Oncotarget
DOI 10.18632/oncotarget.25470PMC PMC5995188
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Figure 1 SEM (A, C) and TEM (B, D) images of mesoporous silica nanomaterials: KCC-Calcined (A, B) and MCM-Calcined (C, D).
Figure 1 SEM (A, C) and TEM (B, D) images of mesoporous silica nanomaterials: KCC-Calcined (A, B) and MCM-Calcined (C, D).CC BY · PubMed Central
Figure 2 DSC profiles of as-synthesized (calcined) MSNs, FITC-labeled MSNs, FA-conjugated MSNs, drug-loaded FA-conjugated MSNs, and pure prodrugs
Figure 2 DSC profiles of as-synthesized (calcined) MSNs, FITC-labeled MSNs, FA-conjugated MSNs, drug-loaded FA-conjugated MSNs, and pure prodrugsCC BY · PubMed Central
Figure 3 XRD patterns of FA-conjugated MSNs, drug-loaded FA-conjugated MSNs, and physical mixtures (P.M.) materials (simple mixing of drug with MSNs)
Figure 3 XRD patterns of FA-conjugated MSNs, drug-loaded FA-conjugated MSNs, and physical mixtures (P.M.) materials (simple mixing of drug with MSNs)CC BY · PubMed Central
Figure 4 FT-IR spectra of: (A) as-synthesized (calcined) MSNs, amino-modified MSNs, and FITC-labeled MSNs (B); CR-loaded to FA-conjugated MSNs (B); QR-loaded FA-conjugated MSNs (C); and COL-loaded FA-conjugated MSNs COL-loaded to FA-conjugated MSNs (D).
Figure 4 FT-IR spectra of: (A) as-synthesized (calcined) MSNs, amino-modified MSNs, and FITC-labeled MSNs (B); CR-loaded to FA-conjugated MSNs (B); QR-loaded FA-conjugated MSNs (C); and COL-loaded FA-conjugated MSNs COL-loaded to FA-conjugated MSNs (D).CC BY · PubMed Central
Figure 5 Zeta potential measurements of: (A) as-synthesized (calcined) MSNs, amino-functionalized MSNs, FITC-labeled MSNs, and FA-conjugated MSNs (B) prodrug-loaded FA-conjugated MSNs.
Figure 5 Zeta potential measurements of: (A) as-synthesized (calcined) MSNs, amino-functionalized MSNs, FITC-labeled MSNs, and FA-conjugated MSNs (B) prodrug-loaded FA-conjugated MSNs.CC BY · PubMed Central
Figure 6 SEM images of cellular uptake of HeLa cells as a function of surface modification of MSNs after 24-h incubation time MCM-Calcined (A), KCC-Calcined (B), MCM-NH2 (C), KCC-NH2 (D), MCM-NH2-FA (E), and KCC-NH2-FA (F).
Figure 6 SEM images of cellular uptake of HeLa cells as a function of surface modification of MSNs after 24-h incubation time MCM-Calcined (A), KCC-Calcined (B), MCM-NH2 (C), KCC-NH2 (D), MCM-NH2-FA (E), and KCC-NH2-FA (F).CC BY · PubMed Central
Figure 7 Confocal laser scanning microscopy (CLSM) images of cellular uptake of HeLa cells treated with FITC (green fluorescence) dye-labeled MSNs (MCM-FITC and KCC-FITC) as a function of time The cell nucleus was stained with DAPI (blue).
Figure 7 Confocal laser scanning microscopy (CLSM) images of cellular uptake of HeLa cells treated with FITC (green fluorescence) dye-labeled MSNs (MCM-FITC and KCC-FITC) as a function of time The cell nucleus was stained with DAPI (blue).CC BY · PubMed Central
Figure 8 Confocal laser scanning microscopy (CLSM) images of intracellular and drug release in HeLa cells of different forms of CR (green fluorescence) as an anticancer prodrug as a function of time Vertical columns show free form, CR-loaded amino-functionalized MSNs (MCM-CR = denotes MCM-NH2-CR and KCC-CR = denotes KCC-NH2-CR), and CR-loaded FA-conjugated MSNs (MCM-FA-CR = denotes MCM-NH2-FA-CR and KCC-FA-CR = denotes KCC-NH2-FA-CR). The cell nucleus was stained with DAPI (blue). The release of CR prodrug can be seen by red arrows. Arrows indicate CR release after MSNs internalization.
Figure 8 Confocal laser scanning microscopy (CLSM) images of intracellular and drug release in HeLa cells of different forms of CR (green fluorescence) as an anticancer prodrug as a function of time Vertical columns show free form, CR-loaded amino-functionalized MSNs (MCM-CR = denotes MCM-NH2-CR and KCC-CR = denotes KCC-NH2-CR), and CR-loaded FA-conjugated MSNs (MCM-FA-CR = denotes MCM-NH2-FA-CR and KCC-FA-CR = denotes KCC-NH2-FA-CR). The cell nucleus was stained with DAPI (blue). The release of CR prodrug can be seen by red arrows. Arrows indicate CR release after MSNs internalization.CC BY · PubMed Central
Figure 9 In vitro cytotoxicity and biocompatibility evaluation of anticancer natural prodrugs suspended in PBS buffer against HepG2 and HeLa cancer cells for 24 h of incubation (A) Biocompatibility of calcined MSNs and amino-functionalized MSNs with concentrations up to 750 µg/ml in HepG2 cells; (B) Biocompatibility of calcined MSNs and amino-functionalized MSNs with concentrations up to 750 µg/ml in HeLa cells; (C) cytotoxicity of pure CR and its nanoformulations in HepG2 cells; (D) cytotoxicity of QR and its nanoformulations in HepG2 cells; (E) cytotoxicity of COL and its nanoformulations; and (F) cytotoxicity of pure CR and its nanoformulations in HeLa cells. Notes: Data are expressed as mean and error bars represent ± standard deviation; *p < 0.05 compared to samples under same concentration; #p < 0.05 compared to concentration of 1 µg/ml (as control).
Figure 9 In vitro cytotoxicity and biocompatibility evaluation of anticancer natural prodrugs suspended in PBS buffer against HepG2 and HeLa cancer cells for 24 h of incubation (A) Biocompatibility of calcined MSNs and amino-functionalized MSNs with concentrations up to 750 µg/ml in HepG2 cells; (B) Biocompatibility of calcined MSNs and amino-functionalized MSNs with concentrations up to 750 µg/ml in HeLa cells; (C) cytotoxicity of pure CR and its nanoformulations in HepG2 cells; (D) cytotoxicity of QR and its nanoformulations in HepG2 cells; (E) cytotoxicity of COL and its nanoformulations; and (F) cytotoxicity of pure CR and its nanoformulations in HeLa cells. Notes: Data are expressed as mean and error bars represent ± standard deviation; *p < 0.05 compared to samples under same concentration; #p < 0.05 compared to concentration of 1 µg/ml (as control).CC BY · PubMed Central
Figure 10 Molecular signaling pathways of CR-loaded FA-conjugated KCC-1 MSN (KCC-NH2-FA-CR) nanoformulation, pure CR, and KCC-NH2-FA MSNs on human HCC cells (HepG2) (A) caspase-3 activation for apoptosis pathway; (B) H2O2 intracellular expression; (C) c-MET inhibition; and (D) MCL-1 inhibition after treatments. Data are expressed as mean and error bars represent ± standard deviation; significance at p < 0.05 compared to negative control (HepG2 cells) and positive control (KCC-NH2-FA nanoparticles). In A and B, * is least significant and ** indicates high significance. In C and D, * is least significant, ** indicates medium significance and *** a very significant effect compared to KCC-NH2-FA nanoparticles as control sample.
Figure 10 Molecular signaling pathways of CR-loaded FA-conjugated KCC-1 MSN (KCC-NH2-FA-CR) nanoformulation, pure CR, and KCC-NH2-FA MSNs on human HCC cells (HepG2) (A) caspase-3 activation for apoptosis pathway; (B) H2O2 intracellular expression; (C) c-MET inhibition; and (D) MCL-1 inhibition after treatments. Data are expressed as mean and error bars represent ± standard deviation; significance at p < 0.05 compared to negative control (HepG2 cells) and positive control (KCC-NH2-FA nanoparticles). In A and B, * is least significant and ** indicates high significance. In C and D, * is least significant, ** indicates medium significance and *** a very significant effect compared to KCC-NH2-FA nanoparticles as control sample.CC BY · PubMed Central
Figure 11 Schematic representation of the prepared nano-system from preparation, internalization, and anticancer mechanism of action in human liver carcinoma (HepG2) cells This schematic shows the prodrug release into cancer cells and the main anticancer action for inducing apoptosis via activation of caspase-3 for killing HepG2 cancer cells, proposed by assistance from important signaling pathways (c-MET, MCL-1, and H2O2).
Figure 11 Schematic representation of the prepared nano-system from preparation, internalization, and anticancer mechanism of action in human liver carcinoma (HepG2) cells This schematic shows the prodrug release into cancer cells and the main anticancer action for inducing apoptosis via activation of caspase-3 for killing HepG2 cancer cells, proposed by assistance from important signaling pathways (c-MET, MCL-1, and H2O2).CC BY · PubMed Central

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Metadata

Authors
AbouAitah, K., Swiderska-Sroda, A., Farghali, A. A., Wojnarowicz, J., Stefanek, A., Gierlotka, S., Opalinska, A., Allayeh, A. K., Ciach, T., & Lojkowski, W.
Affiliations
  • Department of Medicinal and Aromatic Plants Research, Pharmaceutical and Drug Industries Research Division, National Research Centre (NRC), Dokki, Giza, Egypt
  • Laboratory of Nanostructures, Institute of High Pressure Physics, Polish Academy of Sciences, Warsaw, Poland
  • Materials Science and Nanotechnology Department, Faculty of Postgraduate Studies for Advanced Sciences, Beni-Suef University, Beni-Suef, Egypt
  • Biomedical Engineering Laboratory, Faculty of Chemical and Process Engineering, Warsaw University of Technology, Warsaw, Poland
  • Environmental Virology Laboratory, National Research Centre (NRC), Dokki, Giza, Egypt
Venue
Oncotarget
Publisher
Impact Journals, LLC
Published
2018-05-29
Volume
9
Issue
41
Pages
26466-26490
ISSN
1949-2553
DOI
10.18632/oncotarget.25470
PMC
PMC5995188
Cited by
83
References
2
Language
en

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