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. 2021 Dec 14;11:23984. doi: 10.1038/s41598-021-02697-y

Table 2.

Autophagic genes involved in invasion (colonization, proliferation, tumor formation, promotion, metastasis) VS our findings.

Gene expression changes Cellular outcome Effect(s) Consequences on tumor fate References Our study findings
43 °C 48 °C
ATG5 and ATG7- RAS Increased autophagy Mitochondria activation Tumor formation 4,43 2.63 2.94
2.17 NSC
ATG16L1 Autophagy deficiency Oxidative stress Tumor suppression 79,80 1346.5 1164.1
LC3-II degradation Damaged mitochondria
Inflammation induction (1β, IL-18) 2.05 4.58
Autophagy activation p27Kip1 coaded by CDKN1B CDK-dependent kinase inhibitor Tumor promotion 81 423.14 134.83
Autophagy deactivation ATG3/7/p62 targeting Pfkfb3 normal expression Tumor re-proliferation 82 NSC NSC
2.17 NSC
STAT1 inhibition p27 (CDKN1B), p21(CDKN1A) upregulation Increase in IDO1 and Kyn receptors Tumor dormancy 83 423.1 134.8
Rb hypophosphorylation Increase in colony formation
Suppress E2F transcription factor activity Decrease in proliferation
AMBRA1 AMBRA1 role in the modulation of C-MYC phosphorylation and stability Intracellular switch between autophagy and apoptosis Colony formation 84,85 NSC 2.05
ATG9B mutation Autophagy suppression Blocked recruitment of p62-associated ubiquitinated protein for autophagosome–lysosome degradation Tumorigenesis 64,86 2.44 4.07
GABARAPL1 down-regulation Disruption of the intracellular transport of receptors and the autophagy pathway Low GABARAPL1 expression was correlated with a high risk of metastasis Metastasis 87 2.04 NSC
ATG10 up-regulation Acts as an E2-like enzyme that catalyzes the conjugation of ATG12 to ATG5 and increased autophagy Lymphovascular invasion Metastasis 88 2.27 5.05
RAB24 over-expression Promote the EMT, adhesion and vasculogenic effects Promotes the malignant phenotype Tumor growth, metastasis, EMT activation 88 2.76 2.23
ATG5 frameshift mutations Features of cancers with microsatellite instability (MSI) Common in gastric and colorectal carcinomas Tumor development by autophagy deregulation 64 2.63 2.94
CTSB Dormancy hub gene Strong biomarker for GBM patient’s survival Tumor progression 89 10.98 9.68
Metastasis
CXCR4 activation Independent prognostic factor for disease relapse and survival in acute myeloid leukemia (AML) patients Increases autophagic activity and decreases Survival 67,90 NSC 3.64
Colony formation
Cytarabine-induced apoptosis Proliferation
IGF-1 activation Activated protein kinase B (AKT) Inhibit autophagy Induce apoptosis in drug resistant cells 91,92 2.80 2.05
INS over-expression Precursor of insulin Insulin signaling and the regulation of autophagy are relevant to neurodegenerative disorders Survival 93 7.81 15.51
MAPK8 Integration point of proliferation, differentiation, transcription regulation and development Indispensable for TNF superfamily 10 (TNFSF)-induced autophagy Tumor promotion 94 2.96 NSC
Survival
PIK3CG Catalytic subunit of class I PI3Ks Up-regulated under stress conditions Cell remodeling and tissue failure 95 9.42 71.92
MAPK14 Activation of MAPK14 impairs autophagosome–lysosome fusion Phosphorylates ATG5 at threonine 75 Survival promoting autophagy 96,97 2.05 2.23
Cell proliferation
Migration, Resistance to apoptosis
RPS6KB1 In response to mTOR Autophagy inhibition Promote protein synthesis 98 NSC 2.08
Cell growth
Cell proliferation
DRAM2 Is a lysosomal protein DRAM2 overexpression induced cell migration proteins including RAC1, RHOA, RHOC, ROCK1, and decreased RHOB expression Metastasis 99,100 2.05 NSC
Proliferation
Migration
Cell cycle activation
LAMP1 LAMP1 is lysosomal marker LAMP1 overexpression reversed the antitumor effects of UBL4A in pancreatic cancer Cell proliferation 101,102 3.64 3.08
Migration
Invasion
mTOR Key regulator of protein synthesis via 4EBP1 and p70S6K1/2 phosphorylation Increases the translational capacity of cancer cells Autophagy inhibition 103 6.04 6.48
Dormancy
Metastasis
RPLP0 Belongs to the L10P family of ribosomal proteins Affected p21 expression Cell promotion 104,105 NSC 619.5
Induction Autophagy induction (Survival) in response to RPLP deficiency stress
G1 arrest of gastric cancer cells
CTSS Is a lysosomal cysteine protease that may participate in the degradation of antigenic proteins Cleaves some extracellular matrix (ECM) proteins Tumorigenesis stimulation 106,107 11.35 NSC
Metastasis
ESR1 Point mutations on ESR1 are drivers for resistance, and promote of ERα without the bound ligand Ligand independently ER stimulation Proliferation 108,109 9.68 4.16
Long-distance metastasis
Autophagy manipulation eIF4E/eIF4GI knockdown The decrease in ERα, SMAD5, NFkB, CyclinD1, c-MYC, and HIF1α The decrease in EMT promoter 59 1049.1 1904
Increase in EMT inhibitors
The decrease in migration capability

Significant values are in bold. NSC non significant change.