Journal: American Journal of Cancer Research

Article Title: Gentian violet induces apoptosis and ferroptosis via modulating p53 and MDM2 in hepatocellular carcinoma

doi:

Figure Lengend Snippet: GV simultaneously increased the expression levels of MDM2 and p53. A. SK-HEP-1 and SMMC-7721 cells were treated without or with GV at the concentration of 50, 100 nM or 150, 300 nM respectively, for 48 h. Immunoblot was carried out with the indicated antibodies. B. qRT-qPCR results showing the relative fold changes of MDM2 and p53 mRNA expression at the same treatment condition. C. Representative images of the H&E staining, and the p53 and MDM2 immunohistochemical (IHC) staining of the xenograft tumor tissues. Data were presented as mean ± SD. **p<0.01.

Article Snippet: Knockdown of MDM2, p53 and Hep27 was performed using siRNA technology. siRNA oligos targeting MDM2 (sc-29394), p53 (sc-29435), Hep27 (sc-92153) or non-specific siRNAs were purchased from Santa Cruz Biotechnology (Dallas, TX). siRNAs were transfected into cells by electroporation using Nucleofector Device and the Nucleofector Kit L (Lonza, Basel, Switzerland).

Techniques: Expressing, Concentration Assay, Western Blot, Staining, Immunohistochemical staining, Immunohistochemistry

Journal: American Journal of Cancer Research

Article Title: Gentian violet induces apoptosis and ferroptosis via modulating p53 and MDM2 in hepatocellular carcinoma

doi:

Figure Lengend Snippet: The high expression of MDM2 and p53 was dependent on Hep27. Western blot detection of MDM2, p53 and Hep27 expression in SK-HEP-1 and SMMC-7721 cells at the indicated treatment conditions for 48 h. From left to right for each cell line: DMSO, GV (100 nM for SK-HEP-1 and 300 nM for SMMC-7721), GV in cells transfected with Hep27 siRNA, GV co-treated with Fer-1 (2 μM).

Article Snippet: Knockdown of MDM2, p53 and Hep27 was performed using siRNA technology. siRNA oligos targeting MDM2 (sc-29394), p53 (sc-29435), Hep27 (sc-92153) or non-specific siRNAs were purchased from Santa Cruz Biotechnology (Dallas, TX). siRNAs were transfected into cells by electroporation using Nucleofector Device and the Nucleofector Kit L (Lonza, Basel, Switzerland).

Techniques: Expressing, Western Blot, Transfection

Journal: American Journal of Cancer Research

Article Title: Gentian violet induces apoptosis and ferroptosis via modulating p53 and MDM2 in hepatocellular carcinoma

doi:

Figure Lengend Snippet: The proposed molecular mechanisms of GV-induced killing of HCC. When NOX is inhibited by GV, Hep27 is increased, which leads to the blockade of the ubiquitination and degradation of p53 by MDM2. Consequently, the levels of p53 and MDM2 are increased. GV also directly increases p53 level. Increased p53 and MDM2 levels trigger ferroptosis and mitochondrial apoptosis (through the activation of caspase 8) by a coordinated ROS cross point and downstream signaling cascades. On the other hand, GV also triggers death receptor apoptosis (through the activation of caspase 9) by upregulating death receptors DR4/5 and ligands FAS-ligand and TRAIL.

Article Snippet: Knockdown of MDM2, p53 and Hep27 was performed using siRNA technology. siRNA oligos targeting MDM2 (sc-29394), p53 (sc-29435), Hep27 (sc-92153) or non-specific siRNAs were purchased from Santa Cruz Biotechnology (Dallas, TX). siRNAs were transfected into cells by electroporation using Nucleofector Device and the Nucleofector Kit L (Lonza, Basel, Switzerland).

Techniques: Ubiquitin Proteomics, Activation Assay

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: RASSF10 is Epigenetically Inactivated and Suppresses Cell Proliferation and Induces Cell Apoptosis by Activating the p53 Signalling Pathway in Papillary Thyroid Carcinoma Cancer.

doi: 10.1159/000464386

Figure Lengend Snippet: Fig. 5. RASSF10 and p53 regulated PTC cell apoptosis. Apoptosis was determined using flow cytometry analysis of Annexin V/PI double-stained K1 cells. *P < 0.05 versus control group, #P < 0.05 versus RASSF10 group.

Article Snippet: Expression vector construction and transfection The open reading frame (ORF) of the RASSF10 gene was generated by RT-PCR, and p53 siRNA and shRASSF10 were purchased from OriGene Technologies (Rockville, USA).

Techniques: Flow Cytometry, Staining, Control

Journal: Scientific Reports

Article Title: LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway

doi: 10.1038/s41598-017-00913-2

Figure Lengend Snippet: Low frequency MF up-regulated the expression of miR-34a by stabilizing p53 protein. ( A ) Q-PCR analyzes the mRNA levels of P53 in LLC cells treated with MF or Sham MF. ( B ) Protein level of P53 in LLC cells treatment with MF or Sham MF was detected using western Blot. ( C ) The mRNA levels of P53 in LLC cells transfected with siRNA-P53 was detected using Q-PCR. ( D ) Protein level of P53 in LLC cells transfected with siRNA-P53 was detected using western Blot. Numbers under each blot are relative intensity of the blot. (E ) Q-PCR analyzes the miR-34a level after treatment of siRNA-TP53 and H2O2. ( F ) P53 expression in tumor tissue of LLC murine model was detected using IHC staining; Scale bars, 100 µm. ( G ) IHC images were calculated using Image Pro Plus software 6.0 and bar graphs. All experiments were repeated three times. Data represent Mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: P53 specific siRNAs were purchased from RiboBio (Guangzhou, China).

Techniques: Expressing, Western Blot, Transfection, Immunohistochemistry, Software

Journal: Scientific Reports

Article Title: LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway

doi: 10.1038/s41598-017-00913-2

Figure Lengend Snippet: Low frequency MF stabilized p53 protein via inducing cell iron metabolism dysfunction. A549 and LLC cells were pre-incubated with medium containing FAC (100 uM) for 24 h and were exposure to MF or Sham MF for 6 days. ( A ) Protein level of P53 in LLC cells was detected using western blot. Numbers under each blot are relative intensity of the blot. ( B ) Protein expression of TfR and ferritin in LLC cells were detected using western blot. Numbers under each blot are relative intensity of the blot. ( C , D ) Cell proliferation of A549 cells and LLC cells was detected using CCK-8 assay. ( E , F ) Cell cycle of A549 and LLC cells were detected using flow cytometery. ( G , H ) Mean cell proportion in each phase was shown. ( I , J ) Representative image of SA-β-Gal staining assay was showed and numbers of SA-β-Gal positive cells was calculated. All experiments were repeated three times. Data represent Mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: P53 specific siRNAs were purchased from RiboBio (Guangzhou, China).

Techniques: Incubation, Western Blot, Expressing, CCK-8 Assay, Staining

Journal: Theranostics

Article Title: Glucose homeostasis controls N-acetyltransferase 10-mediated ac4C modification of HK2 to drive gastric tumorigenesis

doi: 10.7150/thno.104310

Figure Lengend Snippet: NAT10-mediated ac4C modification of HK2 mRNA maintains its stability. (A) The distribution of ac4C-containing peaks across mRNAs in NAT10-overexpressing (left panel) and NAT10 knockout (right panel) GC cells is displayed in a metagene plot. (B) Representative pie chart of the peak distribution showing the proportions of total ac4C peaks in the indicated regions, including the 5′-untranslated region (5′-UTR), coding sequence (CDS), 3′- untranslated region (3′-UTR), start codon, and stop codon. (C) Consensus motif in AGS WT and NAT10-knockout cells identified by HOMER. (D) Venn diagram showing HK2 as the selected candidate target gene of NAT10. (E) The mRNA level of HK2 in NAT10-overexpressing and NAT10-KO GC cells was measured by qRT-PCR. (F) The protein level of HK2 in NAT10-overexpressing and NAT10-KO GC cells was measured by Western blotting. (G) Sections of xenograft tumors derived from NAT10-overexpressing (upper panel) and NAT10-knockdown (bottom panel) GC cells subcutaneously injected into nude mice were stained with an anti-HK2 antibody for IHC analysis (scale bars = 50 μm). (H) Sections of organoids formed from cells transduced with the NAT10 overexpression or control lentiviral vector were subjected to H&E staining or IHC staining with an anti-HK2 antibody (scale bars = 50 μm). (I) Sections of stomachs from NAT10 WT and cKO mice were stained with an anti-HK2 antibody for IHC analysis (scale bars = 100 μm). (J) Integrative Genomics Viewer (IGV) tracks revealing the ac4Cseq read distribution on HK2 mRNA in NAT10-overexpressing and NAT10-knockout GC cells. (K) acRIP-qPCR analysis was employed to demonstrate the presence of NAT10-mediated HK2 ac4C modifications. ac4C modification of HK2 was increased upon overexpression of NAT10, while it was decreased upon knockout of NAT10. (L) The level of HK2 expression in NAT10-overexpressing, NAT10-knockout and the corresponding control GC cells treated with actinomycin D (2 μg/mL) at the indicated time points was measured by qRT-PCR. (M) Schematic representation of the construction of the luciferase reporter vectors containing the HK2 WT, Mut1, Mut2, or Both Mut sequences (left panel). The relative luciferase activities of the HK2 WT, Mut1, Mut2, and Both Mut luciferase reporters in AGS cells with NAT10 knockout and the corresponding control cells were measured (right panel). H&E, haematoxylin and eosin; IHC, immunohistochemical; GC, gastric cancer; WT, wild type; KO, knockout. The statistical data in this figure are presented as the mean values ± SDs of three independent experiments. Statistical significance was determined by a two-tailed t test. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: siRNAs targeting NAT10 or HK2 were designed and synthesized by RiboBio (Guangzhou, China).

Techniques: Modification, Knock-Out, Sequencing, Quantitative RT-PCR, Western Blot, Derivative Assay, Knockdown, Injection, Staining, Transduction, Over Expression, Control, Plasmid Preparation, Immunohistochemistry, Expressing, Luciferase, Immunohistochemical staining, Two Tailed Test

Journal: Theranostics

Article Title: Glucose homeostasis controls N-acetyltransferase 10-mediated ac4C modification of HK2 to drive gastric tumorigenesis

doi: 10.7150/thno.104310

Figure Lengend Snippet: NAT10 accelerates malignant progression of GC by upregulating HK2. (A) The HK2 protein level was measured in GC tissues and paired normal gastric mucosal tissues by Western blotting (n = 5). (B) Representative IHC images of the tissue microarray analysed with the anti-HK2 antibody (scale bars = 200 or 100 μm) are shown (left panel). The distribution of the difference in the HK2 immunoreactivity score (IRS) (△IRS = IRST - IRSN) is shown. The IRS for HK2 staining was available for 192 pairs of tissues. (C) Representative images of HK2 IHC staining in tissues from GC patients in the SUVmax-high and SUVmax-low groups (left panel). Scale bars = 50 μm; n = 22; statistical analysis of the difference in HK2 expression between the SUVmax-high group and the SUVmax-low group (right panel). (D) Correlation analysis between the SUVmax and HK2 protein expression level based on the IHC score in GC tissue microarrays with associated PET/CT data. R, Pearson correlation coefficient; n = 22. (E) Kaplan-Meier analysis of OS in GC patients stratified by HK2 expression (n = 192, P = 6.4e-15; log-rank test). (F) Multivariate analyses were performed for the GC cohort. (G) Glucose uptake (left panel) and lactate production (right panel) in HK2-knockdown AGS cells were measured. (H) A colony formation assay was performed in stable HK2-knockdown AGS cells (left panel). Quantitative analysis of the colony formation assay results (right panel). (I) NAT10 expression was positively correlated with HK2 protein expression in GC tissues (linear regression) according to analysis of the IHC score from the TMA data (n = 192). (J) Correlation analysis of NAT10 and HK2 protein expression based on the IHC score in GC tissue microarrays with associated PET/CT data (n = 22). (K) The colony formation ability was evaluated in NAT10-overexpressing BGC823 cells with or without stable HK2 knockdown or the corresponding controls. Representative images (left panel) and quantitative results (right panel) are shown. (L) Lactate production was measured in NAT10-overexpressing BGC823 cells with or without stable HK2 knockdown or the corresponding controls. CI, confidence interval; GC, gastric cancer; HR, hazard ratio; IHC, immunohistochemical; OS, overall survival; TNM, tumor, node, metastasis. The statistical data in this figure are presented as the mean value ± SD of three independent experiments. Statistical significance was determined by a two-tailed t test. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: siRNAs targeting NAT10 or HK2 were designed and synthesized by RiboBio (Guangzhou, China).

Techniques: Western Blot, Microarray, Staining, Immunohistochemistry, Expressing, Positron Emission Tomography-Computed Tomography, Knockdown, Colony Assay, Immunohistochemical staining, Two Tailed Test

Journal: Theranostics

Article Title: Glucose homeostasis controls N-acetyltransferase 10-mediated ac4C modification of HK2 to drive gastric tumorigenesis

doi: 10.7150/thno.104310

Figure Lengend Snippet: Targeting the NAT10-HK2 axis in GC cells has clinical value. (A) Different GC cell lines were treated with 10 μM remodelin for 24 h. Then, the protein level of NAT10 was measured by Western blot analysis (upper panel). mRNA isolated from GC cells were subjected to dot blot analysis with an anti-ac4C antibody (bottom panel). MB staining served as a loading control. (B) Glucose uptake (left panel) and lactate production (right panel) were measured in MKN45 cells after treatment with 10 μM Remodelin for 24 h. (C) Remodelin inhibited subcutaneous tumor growth in nude mice (n = 6, left panel). The tumor volume was monitored every other day, and tumor growth curves were generated (middle panel). The tumors were extracted and weighed after 25 days (right panel). (D) Sections of tumors were stained with anti-Ki-67, anti-HK2, and anti-NAT10 antibodies for IHC analysis (scale bars = 50 μm). (E) Representative images of GC organoids treated with 10 μM Remodelin for the indicated durations (scale bars = 100 μm, left panel) and quantification of organoid diameters (right panel). (F) Sections of organoids treated with Remodelin were subjected to H&E staining or stained with anti-Ki-67, anti-HK2, and anti-NAT10 antibodies for IHC analysis (scale bars = 50 μm). (G) The combination of NAT10 and HK2 was evaluated as a new two-gene risk signature, and multivariate analyses were performed for the GC cohort. (H) GC patients were divided into three subgroups according to the median expression level of each protein: high expression of both NAT10 and HK2, low expression of both NAT10 and HK2, and other expression patterns (NAT10 high and HK2 low OR NAT10 low and HK2 high). Kaplan-Meier analysis of survival in the three subgroups of GC patients. (I) Time-dependent receiver operating characteristic (ROC) curve analysis of the NAT10 risk score, the HK2 risk score, and the combined NAT10/HK2 score in the GC cohort. AUC, area under the curve; CI, confidence interval; GC, gastric cancer; HR, hazard ratio; IHC, immunohistochemical; OS, overall survival; TNM, tumor, node, metastasis. (J) Graphical illustration of the mechanism by which NAT10 modulates glycolysis, promoting GC growth. The statistical data in this figure are presented as the mean value ± SD of three independent experiments. Statistical significance was determined by a two-tailed t test. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: siRNAs targeting NAT10 or HK2 were designed and synthesized by RiboBio (Guangzhou, China).

Techniques: Western Blot, Isolation, Dot Blot, Staining, Control, Generated, Expressing, Immunohistochemical staining, Two Tailed Test

Journal: Frontiers in Physiology

Article Title: The Oncogenic Role of Tribbles 1 in Hepatocellular Carcinoma Is Mediated by a Feedback Loop Involving microRNA-23a and p53

doi: 10.3389/fphys.2017.00789

Figure Lengend Snippet: TRIB1 is overexpressed in human HCC tissues and cell lines. (A) qRT-PCR analysis of TRIB1 and p53 mRNA expression in HCC tumors and adjacent non-tumor tissues. (B) We have made a pooled dot plot to verify the correlation again in HCC patients. (C) Immunohistochemical analysis of TRIB1 in HCC (left panel) and adjacent liver tissues (right panel) (original magnification, × 200). (D) Western blot analysis of TRIB1 protein expression in the normal liver cell line LO2 and the HCC cell lines SMMC-7721, HepG2, and Huh 7. β-actin was used as an internal control. (E) qRT-PCR analysis of TRIB1 and p53 mRNA expression in HCC and normal liver cells. The data were normalized to the expression levels in LO2 cells. Bar graphs (mean ± SEM) and representative images are shown. * p < 0.05, ** p < 0.01 compared with the LO2 group ( n = 3).

Article Snippet: Expression vectors encoding the TRIB1 or p53 genes, and small interfering RNA (siRNA) against TRIB1 or p53 were purchased from Shanghai GenePharma Co. Ltd. (Shanghai, China).

Techniques: Quantitative RT-PCR, Expressing, Immunohistochemical staining, Western Blot, Control

Journal: Frontiers in Physiology

Article Title: The Oncogenic Role of Tribbles 1 in Hepatocellular Carcinoma Is Mediated by a Feedback Loop Involving microRNA-23a and p53

doi: 10.3389/fphys.2017.00789

Figure Lengend Snippet: TRIB1 downregulates p53 and promotes HCC cell growth. (A–D) The mRNA and protein expression levels of TRIB1 and p53 in HepG2 (A,C) and Huh7 (B,D) cells treated with or without siTRIB1 or negative control (siNC) or TRIB1 plasmid were determined by qRT-PCR and western blotting. * p < 0.05 or ** p < 0.01, compared with the control group. Immunocytochemistry were used to detect the p53 and TRIB1 expression in (E) HepG2 cells and (F) Huh7 (Y220C) cells. Cell growth of HepG2 (G) and Huh7 (H) cells treated as described above was determined using the MTT assay at the indicated time points. * p < 0.05 or ** p < 0.01, compared with the control group ( n = 3).

Article Snippet: Expression vectors encoding the TRIB1 or p53 genes, and small interfering RNA (siRNA) against TRIB1 or p53 were purchased from Shanghai GenePharma Co. Ltd. (Shanghai, China).

Techniques: Expressing, Negative Control, Plasmid Preparation, Quantitative RT-PCR, Western Blot, Control, Immunocytochemistry, MTT Assay

Journal: Frontiers in Physiology

Article Title: The Oncogenic Role of Tribbles 1 in Hepatocellular Carcinoma Is Mediated by a Feedback Loop Involving microRNA-23a and p53

doi: 10.3389/fphys.2017.00789

Figure Lengend Snippet: miR-23a regulates the TRIB1/p53 axis in HCC cells. (A–C) The expression levels of p53, TRIB1, and miR-23a were examined in HCC cells transfected with or without a p53 overexpression plasmid by qRT-PCR. (D) TRIB1 is a predicted target of miR-23a by TargetScan. (E) HepG2 cells were co-transfected with miR-23a and wild-type (wt) or mutant (mut) pGL3-TRIB1 constructs and subjected to luciferase reporter assays. (F,G) The expression levels of TRIB1 and p53 in HepG2 cells transfected with or without miR-NC or miR-23a were determined by qRT-PCR and western blotting. (H) Schematic showing the miR-23a/TRIB1/p53 feed-forward loop ( n = 3). * p < 0.05, ** p < 0.01 compared with the control group.

Article Snippet: Expression vectors encoding the TRIB1 or p53 genes, and small interfering RNA (siRNA) against TRIB1 or p53 were purchased from Shanghai GenePharma Co. Ltd. (Shanghai, China).

Techniques: Expressing, Transfection, Over Expression, Plasmid Preparation, Quantitative RT-PCR, Mutagenesis, Construct, Luciferase, Western Blot, Control

Journal: Frontiers in Physiology

Article Title: The Oncogenic Role of Tribbles 1 in Hepatocellular Carcinoma Is Mediated by a Feedback Loop Involving microRNA-23a and p53

doi: 10.3389/fphys.2017.00789

Figure Lengend Snippet: TRIB1 stimulates β-catenin signaling in a p53-dependent manner. (A) The expression of β-catenin, c-Myc, and MMP7 was detected by western blotting in HepG2 and Huh-7 cells transfected with siNC or siTRIB1 or Vector or TRIB1. β-actin was used as a loading control. * p < 0.05, ** p < 0.01 compared with the siNC group ( n = 3). (B) Effect of p53 and TRIB1 silencing on β-catenin expression in HepG2 and Huh-7 cells was detected by western blotting. * p < 0.05, ** p < 0.01 compared with the siNC[siP53(−)] group ( n = 3).

Article Snippet: Expression vectors encoding the TRIB1 or p53 genes, and small interfering RNA (siRNA) against TRIB1 or p53 were purchased from Shanghai GenePharma Co. Ltd. (Shanghai, China).

Techniques: Expressing, Western Blot, Transfection, Plasmid Preparation, Control

Journal: Frontiers in Physiology

Article Title: The Oncogenic Role of Tribbles 1 in Hepatocellular Carcinoma Is Mediated by a Feedback Loop Involving microRNA-23a and p53

doi: 10.3389/fphys.2017.00789

Figure Lengend Snippet: TRIB1 knockdown inhibits in vivo tumor formation from HepG2 cells in nude mice. Stable TRIB1 knockdown and control HepG2 cells were implanted subcutaneously in the left flank of nude mice. (A) After 35 days, mice were sacrificed and tumors were excised. (B) Effect of TRIB1 knockdown on tumor volume in a nude mice model. (C) The TUNEL assay (×400) was performed to determine the apoptotic indices. (D) Western blot analysis of the expression of p53, β-catenin, and c-myc in tumor tissues from control and shTRIB1 mice. β-actin was used as an internal control. Bar graphs (mean ± SEM) and representative images are shown. * p < 0.05, ** p < 0.01 compared with the control group ( n = 3).

Article Snippet: Expression vectors encoding the TRIB1 or p53 genes, and small interfering RNA (siRNA) against TRIB1 or p53 were purchased from Shanghai GenePharma Co. Ltd. (Shanghai, China).

Techniques: Knockdown, In Vivo, Control, TUNEL Assay, Western Blot, Expressing

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Engineering Nanoparticles for Targeted Delivery of Nucleic Acid Therapeutics in Tumor

doi: 10.1016/j.omtm.2018.09.002

Figure Lengend Snippet: The siRNA/MicroRNA-Based Drugs Targeting Different Diseases in Clinical Trials

Article Snippet: Glioblastoma , siRNA target p53 , nanoparticle (NPs) , Temozolomide/SGT-53 , SynerGene Therapeutics , NCT02340156.

Techniques: Polymer, Liposomes, shRNA, Plasmid Preparation, Virus, Infection, Injection

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Engineering Nanoparticles for Targeted Delivery of Nucleic Acid Therapeutics in Tumor

doi: 10.1016/j.omtm.2018.09.002

Figure Lengend Snippet: Schematic Illustrations of the siRNA-Based Therapeutics of CALAA-01 and siG12D-LODER (A) CALAA-01 is a polymer-based nanoparticle containing a targeting ligand on its surface (the human protein transferrin) and a small interfering RNA (siRNA) that targets the M2 subunit of ribonucleotide reductase ( RRM2 ). Reproduced with permission from Zuckerman and Davis. Copyright © 2015 Springer Nature. (B) siG12D-LODER is a polymeric matrix of poly(lactic-co-glycolic) acid (PLGA) in a shape of a small cylindrical rod of 0.8 mm in diameter and 5.5 ± 1 mm in length. Reproduced with permission from Titze-de-Almeida et al. Copyright © 2017 Springer Nature.

Article Snippet: Glioblastoma , siRNA target p53 , nanoparticle (NPs) , Temozolomide/SGT-53 , SynerGene Therapeutics , NCT02340156.

Techniques: Polymer, Small Interfering RNA

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Engineering Nanoparticles for Targeted Delivery of Nucleic Acid Therapeutics in Tumor

doi: 10.1016/j.omtm.2018.09.002

Figure Lengend Snippet: The Application of PEI for Co-delivery of siRNA and DOX and the Schematic Synthesis of Folate-PEI-CDs/siRNA Nanoparticles (A) Confocal laser scanning microscope (CLSM) images of B16F10 cells incubated with PEI/siRNA/DOX for 24 hr. Scale bars, 20 μm. Reproduced with permission from Xu et al. Copyright © 2017 Elsevier. (B) Schematic diagram of synthesis route of folate-PEI-CDs/siRNA nanoassemblies. Reproduced with permission from He et al. Copyright © 2017 Elsevier.

Article Snippet: Glioblastoma , siRNA target p53 , nanoparticle (NPs) , Temozolomide/SGT-53 , SynerGene Therapeutics , NCT02340156.

Techniques: Laser-Scanning Microscopy, Incubation