Graphene oxide substrates with N-cadherin stimulates neuronal growth and intracellular transport

Qin, Ellen C.; Kandel, Mikhail E.; Liamas, Evangelos; Shah, Tauseef B.; Kim, Chaeyeon; Kaufman, Collin D.; Zhang, Zhenyu J.; Popescu, Gabriel; Gillette, Martha U.; Leckband, Deborah; Kong, Hyunjoon

doi:10.1016/j.actbio.2019.04.005

Cited by 16 publications

(10 citation statements)

References 54 publications

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“…3 Recent studies have shown that GFNs might also be used as a platform to enhance cellular growth such as that of neuronal cells. 4 However, the potential neurotoxicity of GFNs has also been reported in different biological models such as human neuroblastoma cells (SH-SY5Y), 5 Caenorhabditis elegans, 6 or zebrafish. 7 For example, graphene oxide (100-800 nm) at concentrations higher than 80 mg L −1 can cause neurotoxicity to SH-SY5Y cells.…”

Section: Introductionmentioning

confidence: 99%

Elucidating the mechanism of the surface functionalization dependent neurotoxicity of graphene family nanomaterials

et al. 2020

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Section: Introductionmentioning

confidence: 99%

Elucidating the mechanism of the surface functionalization dependent neurotoxicity of graphene family nanomaterials

et al. 2020

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“…It is the cytoskeleton that helps the cell to maintain its shape and internal organization [33][34][35][36][37]. The changes in the morphology of the cell membrane are due to damage to the cytoskeleton caused by GO [38][39][40][41][42]. This compound interacts with the cell membrane by adhesion.…”

Section: Discussionmentioning

confidence: 99%

Graphene Oxide Nanoparticles Induce Apoptosis in wild-type and CRISPR/Cas9-IGF/IGFBP3 knocked-out Osteosarcoma Cells

et al. 2020

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Osteosarcoma affects both adolescents and adults, and some improvement in the survival rate for affected patients has been reached in the last decade. Still, non-specificity and systemic toxicity may limit traditional therapeutic approaches to some extent. The insulin growth factor 1 (IGF1) and its binding protein (IGFBP3) have been implicated in the tumorigenesis. Nanoparticles, such as graphene oxide (GO), can provide an effective treatment for cancer as they can specifically target cancer cells while reducing undesired side effects. This study aimed to evaluate the toxicity of GO on osteosarcoma in vitro using tumor cell lines with and without knocking out the IGF and IGFBP3 genes. Human osteosarcoma cell lines, U2OS and SAOS2, and the normal osteoblast cell line hFOB1.19 were used. The IGF1 and IGFBP3 genes were eliminated using CRISPR/Cas9. Tumor cells were cultured and treated with GO. Apoptosis and reactive oxygen species (ROS) were analyzed by Annexin V-FITC and ROS assays. The nuclear factor erythroid 2-related factor 2 (NRF2), which is a crucial regulator of cellular resistance to oxidants, was investigated by Western blotting. We found a significantly higher rate of apoptosis in the OS than hFOB1.19, especially in U2OS cells in which IGF1 and IGFBP3 were knocked out. ROS increase due to GO exposure was remarkably time and concentration-dependent. Based on the rate of apoptosis, ROS, Nrf-2 decrease, and cytomorphological changes, GO has a significant cytotoxic effect against OS. Targeting the IGF1 and IGFBP3 signaling pathway may strengthen GO-related cytotoxicity with the potential to increase the survival of patients affected by this tumor.

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“…Recent studies have shown that miR-375 inhibitor treatment can promote EMT of human GC cells, which, in turn, affects carcinogenesis (77). E-cadherin is known to play a vital role in the selective aggregation of cells during growth and development (78). The E-cadherin-mediated cell adhesion and loss of cell connections can cause cells to separate from the primary tumor and migrate to distant sites (79).…”

Section: Mechanism Of Mir-375 In Cancer Metastasismentioning

confidence: 99%

“…E-cadherin is known to play a vital role in the selective aggregation of cells during growth and development [ 78 ]. The E-cadherin-mediated cell adhesion and loss of cell connections can cause cells to separate from the primary tumor and migrate to distant sites [ 79 ].…”

Section: Mechanism Of Mir-375 In Cancer Metastasismentioning

confidence: 99%

MicroRNA-375: potential cancer suppressor and therapeutic drug

Wei

Wang

et al. 2021

Bioscience Reports

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MiR-375 is a conserved noncoding RNA that is known to be involved in tumor cell proliferation, migration, and drug resistance. Previous studies have shown that miR-375 affects the epithelial-mesenchymal transition (EMT) of human tumor cells via some key transcription factors, such as Yes-associated protein 1 (YAP1), Specificity protein 1 (SP1) -and signaling pathways (Wnt signaling pathway, nuclear factor kappa B (NF-kB) pathway and transforming growth factor β (TGF-β) signaling pathway) and is vital for the development of cancer. Additionally, recent studies have identified miRNA delivery system carriers for improved in vivo transportation of miR-375 to specific sites. Here, we discussed the role of miR-375 in different types of cancers, as well as molecular mechanisms, and analyzed the potential of miR-375 as a molecular biomarker and therapeutic target to improve the efficiency of clinical diagnosis of cancer.

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Graphene oxide substrates with N-cadherin stimulates neuronal growth and intracellular transport

Cited by 16 publications

References 54 publications

Elucidating the mechanism of the surface functionalization dependent neurotoxicity of graphene family nanomaterials

Elucidating the mechanism of the surface functionalization dependent neurotoxicity of graphene family nanomaterials

Graphene Oxide Nanoparticles Induce Apoptosis in wild-type and CRISPR/Cas9-IGF/IGFBP3 knocked-out Osteosarcoma Cells

MicroRNA-375: potential cancer suppressor and therapeutic drug

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