Skip to main content
. 2021 Aug 18;13(16):4145. doi: 10.3390/cancers13164145

Table 2.

The role of autophagy modulation in GNM-induced cancer cell death.

GNM Cell Type Type of Cell Death Autophagy Involvement Cell Death Modulation Cell Death Mechanisms Ref.
GO + cisplatin Skov-3 human ovarian carcinoma necrosis cytotoxic autophagy induction ↓ by ULK1 RNAi
↓ by ATG7 RNAi
nuclear import of LC3 [30]
GO + cisplatin CT26 mouse colon carcinoma necrosis cytotoxic autophagy induction ↓ by 3-MA
↓ by BAF A1
nuclear import of LC3 [32]
blue light-excited GQD U251 human glioma apoptosis cytotoxic autophagy induction ↓ by LC3B RNAi ↑ROS, ↑caspases [39]
hydroxy-GQD A549 human lung carcinoma apoptosis cytoprotective autophagy induction ↑ by 3-MA n.a. [40]
amino-GQD A549 human lung carcinoma apoptosis upon autophagy inhibition cytoprotective autophagy induction ↑ by 3-MA n.a. [40]
GO-CQ conjugate A549 human lung carcinoma necroptosis cytotoxic block of autophagic flux ↓ by p62 RNAi ↑ROS, ↑RIPK1, ↑RIPK3, ↑MLKL,
p62 and ATG5 as scaffolds for necrosome assembly
[43]
GO PC12 rat pheochromocytoma apoptosis cytotoxic block of autophagic flux ↓ by rapamycin
↓ by p62 RNAi
↑p62, ↑LMP, ↓ΔΨ, ↑Bax/Bcl-2,
↑caspase-3, ↑caspase-9
[44]
GNF A549 human lung carcinoma apoptosis cytotoxic block of autophagic flux ↓ by 3-MA
↓ by LC3 RNAi
↑ROS, ↑LMP, ↓ΔΨ, ↑Bax/Bcl-2, ↓ATP, ↑caspase-3, ↓actin cytoskeleton [45]
GO F98 rat glioma apoptosis cytotoxic block of autophagic flux ↓ by rapamycin ↑p62, ↑Bax/Bcl-2, ↓ΔΨ, ↑caspase-3 [46]

↑, increase/activation; ↓, decrease/inhibition; n.a., not assessed; ΔΨ, mitochondrial membrane potential; 3-MA, 3-methyladenine; ATG, autophagy-related; BAF, bafilomycin; CQ, chloroquine; CTS, cathepsin; GNF, graphene nanofibers; GO, graphene oxide; GQD, graphene quantum dots; LC3, microtubule-associated light chain 3; LMP, lysosome membrane permeabilization; MLKL, mixed lineage kinase domain-like; RIPK, receptor-interacting protein kinase; ROS, reactive oxygen species; RNAi, RNA interference; ULK, Unc-51-like autophagy activating kinase.