TY - JOUR
T1 - Graphene oxide nanoarchitectures in cancer biology
T2 - Nano-modulators of autophagy and apoptosis
AU - Taheriazam, Afshin
AU - Abad, Ghazaleh Gholamiyan Yousef
AU - Hajimazdarany, Shima
AU - Imani, Mohammad Hassan
AU - Ziaolhagh, Setayesh
AU - Zandieh, Mohammad Arad
AU - Bayanzadeh, Seyedeh Delaram
AU - Mirzaei, Sepideh
AU - Hamblin, Michael R.
AU - Entezari, Maliheh
AU - Aref, Amir Reza
AU - Zarrabi, Ali
AU - Ertas, Yavuz Nuri
AU - Ren, Jun
AU - Rajabi, Romina
AU - Paskeh, Mahshid Deldar Abad
AU - Hashemi, Mehrdad
AU - Hushmandi, Kiavash
N1 - Publisher Copyright:
© 2023 Elsevier B.V.
PY - 2023/2
Y1 - 2023/2
N2 - Nanotechnology is a growing field, with many potential biomedical applications of nanomedicine for the treatment of different diseases, particularly cancer, on the horizon. Graphene oxide (GO) nanoparticles can act as carbon-based nanocarriers with advantages such as a large surface area, good mechanical strength, and the capacity for surface modification. These nanostructures have been extensively used in cancer therapy for drug and gene delivery, photothermal therapy, overcoming chemotherapy resistance, and for imaging procedures. In the current review, we focus on the biological functions of GO nanoparticles as regulators of apoptosis and autophagy, the two major forms of programmed cell death. GO nanoparticles can either induce or inhibit autophagy in cancer cells, depending on the conditions. By stimulating autophagy, GO nanocarriers can promote the sensitivity of cancer cells to chemotherapy. However, by impairing autophagy flux, GO nanoparticles can reduce cell survival and enhance inflammation. Similarly, GO nanomaterials can increase ROS production and induce DNA damage, thereby sensitizing cancer cells to apoptosis. In vitro and in vivo experiments have investigated whether GO nanomaterials show any toxicity in major body organs, such as the brain, liver, spleen, and heart. Molecular pathways, such as ATG, MAPK, JNK, and Akt, can be regulated by GO nanomaterials, leading to effects on autophagy and apoptosis. These topics are discussed in this review to shed some lights towards the biomedical potential of GO nanoparticles and their biocompatibility, paving the way for their future application in clinical trials.
AB - Nanotechnology is a growing field, with many potential biomedical applications of nanomedicine for the treatment of different diseases, particularly cancer, on the horizon. Graphene oxide (GO) nanoparticles can act as carbon-based nanocarriers with advantages such as a large surface area, good mechanical strength, and the capacity for surface modification. These nanostructures have been extensively used in cancer therapy for drug and gene delivery, photothermal therapy, overcoming chemotherapy resistance, and for imaging procedures. In the current review, we focus on the biological functions of GO nanoparticles as regulators of apoptosis and autophagy, the two major forms of programmed cell death. GO nanoparticles can either induce or inhibit autophagy in cancer cells, depending on the conditions. By stimulating autophagy, GO nanocarriers can promote the sensitivity of cancer cells to chemotherapy. However, by impairing autophagy flux, GO nanoparticles can reduce cell survival and enhance inflammation. Similarly, GO nanomaterials can increase ROS production and induce DNA damage, thereby sensitizing cancer cells to apoptosis. In vitro and in vivo experiments have investigated whether GO nanomaterials show any toxicity in major body organs, such as the brain, liver, spleen, and heart. Molecular pathways, such as ATG, MAPK, JNK, and Akt, can be regulated by GO nanomaterials, leading to effects on autophagy and apoptosis. These topics are discussed in this review to shed some lights towards the biomedical potential of GO nanoparticles and their biocompatibility, paving the way for their future application in clinical trials.
KW - Apoptosis
KW - Autophagy
KW - Biocompatibility
KW - Biomedical applications
KW - Cancer therapy
KW - Graphene oxide
UR - http://www.scopus.com/inward/record.url?scp=85146594891&partnerID=8YFLogxK
U2 - 10.1016/j.jconrel.2023.01.028
DO - 10.1016/j.jconrel.2023.01.028
M3 - Review article
C2 - 36641122
AN - SCOPUS:85146594891
SN - 0168-3659
VL - 354
SP - 503
EP - 522
JO - Journal of Controlled Release
JF - Journal of Controlled Release
ER -