Life, death, and autophagy in cancer: NF-κB turns up everywhere

Verzella, Daniela; Pescatore, Alessandra; Capece, Daria; Vecchiotti, Davide; Ursini, Matilde Valeria; Franzoso, Guido; Alesse, Edoardo; Zazzeroni, Francesca

doi:10.1038/s41419-020-2399-y

Cited by 224 publications

(173 citation statements)

References 151 publications

(199 reference statements)

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“…Aberrant NF- κ B signaling is involved in the pathogenesis of most human malignancies. Consequently, it is now used as an important target for cancer therapy [ 20 – 22 ]. CCND1 and c-Myc are proliferation-related genes [ 23 ], and MMP9 and Slug are EMT- (cell migration and invasiveness) related genes downstream of the classical NF- κ B pathway [ 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

Guo

Song

Chang

et al. 2020

Behavioural Neurology

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Objective. Our study was aimed at investigating the mechanistic consequences of the upregulation of adipocyte enhancer-binding protein 1 (AEBP1) in glioblastoma (GBM). Methods. The expression of AEBP1 in GBM was assessed by bioinformatics analysis and qRT-PCR; the effects of AEBP1 on GBM cell proliferation, migration, invasion, and tumor growth in vitro and in vivo were detected by a CCK-8 assay, colony formation assay, scratch assay, Transwell assay, and subcutaneous tumor formation, respectively. The activation of related signaling pathways was monitored using western blot. Results. Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. The results of in vitro experiments showed that AEBP1 could significantly promote GBM cell proliferation, migration, and invasion; in vivo experiments suggested that AEBP1 could contribute to the growth of GBM tumors. AEBP1 could upregulate the level of IκBα phosphorylation, decrease IκBα expression, activate the NF-κB signaling pathway, and promote the expression of downstream oncogenes. Conclusion. Upregulated AEBP1 in GBM promotes GBM cell proliferation, migration, and invasion and facilitates tumor growth in vivo by activating the classical NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

Guo

Song

Chang

et al. 2020

Behavioural Neurology

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“…Prolonged inflammation is associated with an increased risk of cancer, as it favors mismatch repair abnormalities or alters DNA methylation, and DNA hypermethylation has been reported to precede large granular lymphocytic leukemia by activating the NF-κB-Myc axis [15]. NF-κB is activated mainly by mutations of the upstream components of this pathway, as observed in a plethora of hematological as well as solid cancers [41]. Interestingly, NF-κB that promotes the release of pro-inflammatory cytokines may in turn be activated by them, in a regulatory circuit that plays a critical role in cancerogenesis.…”

Section: Cross Talk Between Nf-κb Upr Autophagy and Mutp53mentioning

confidence: 99%

Oncogenic pathways activated by pro-inflammatory cytokines promote mutant p53 stability: clue for novel anticancer therapies

D’Orazi

Cordani

Cirone

2020

Cell. Mol. Life Sci.

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Inflammation and cancerogenesis are strongly interconnected processes, not only because inflammation promotes DNA instability, but also because both processes are driven by pathways such as NF-kB, STAT3, mTOR and MAPKs. Interestingly, these pathways regulate the release of pro-inflammatory cytokines such as IL-6, TNF-α and IL-1β that in turn control their activation and play a crucial role in shaping immune response. The transcription factor p53 is the major tumor suppressor that is often mutated in cancer, contributing to tumor progression. In this overview, we highlight how the interplay between proinflammatory cytokines and pro-inflammatory/pro-oncogenic pathways, regulating and being regulated by UPR signaling and autophagy, affects the stability of mutp53 that in turn is able to control autophagy, UPR signaling, cytokine release and the activation of the same oncogenic pathways to preserve its own stability and promote tumorigenesis. Interrupting these positive feedback loops may represent a promising strategy in anticancer therapy, particularly against cancers carrying mutp53.

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“…2). Inflammatory cytokines can signal through cytokine receptors on transformed cells to increase prosurvival NF-jB-dependent and NF-jB-independent pathways to increase the survival and proliferation of malignant clones [30,50]. Additionally, many proinflammatory cytokines such as IL-6 can increase tumour cell proliferation [51].…”

Section: Inflammation Enhances Tumorigenesismentioning

confidence: 99%

Autophagy, the innate immune response and cancer

Gerada

Ryan

2020

Molecular Oncology

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Both autophagy, a cellular recycling process, and the innate immune response can have different effects on tumour formation at different stages. Interestingly, autophagy and the innate immune response interact during tumorigenesis to have both tumour‐promoting and tumour‐inhibiting affects. By dissecting the interaction between autophagy and the innate immune response during tumour formation, novel therapeutic strategies may be identified.

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Life, death, and autophagy in cancer: NF-κB turns up everywhere

Cited by 224 publications

References 151 publications

AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

Oncogenic pathways activated by pro-inflammatory cytokines promote mutant p53 stability: clue for novel anticancer therapies

Autophagy, the innate immune response and cancer

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