Deleting key autophagy elongation proteins induces acquirement of tumor-associated phenotypes via ISG15

Kong, Eun Bin; Kim, Hag Dong; Kim, Joon

doi:10.1038/s41418-020-0519-y

Cited by 19 publications

(18 citation statements)

References 65 publications

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“…After three washes in PBST, each blot was incubated with peroxidase-conjugated secondary antibody for 1 h at 37°C. Labeled proteins were visualized using the Odyssey infrared scanner (LI-COR, Lincoln, NB, USA) [ 48 ]. Signals were densitometrically assessed and normalized to the β -actin signals, and an enhanced chemiluminescence detection system (Amersham, Piscataway, NJ, USA) was used to visualize the antibody-specific proteins in accordance with the manufacturer's recommended protocol [ 49 ].…”

Section: Methodsmentioning

confidence: 99%

Bevacizumab‐Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity

Tian

Yue

et al. 2021

Oxidative Medicine and Cellular Longevity

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The molecular mechanisms underlying the cardiotoxicity associated with bevacizumab, a first-line immunotherapeutic agent used to treat lung cancer, are not fully understood. Here, we examined intracellular signal transduction in cardiomyocytes after exposure to different doses of bevacizumab in vitro. Our results demonstrated that bevacizumab significantly and dose-dependently reduces cardiomyocyte viability and increases cell apoptosis. Bevacizumab treatment also led to mitochondrial dysfunction in cardiomyocytes, as evidenced by the decreased ATP production, increased ROS production, attenuated antioxidative enzyme levels, and reduced respiratory complex function. In addition, bevacizumab induced intracellular calcium overload, ER stress, and caspase-12 activation. Finally, bevacizumab treatment inhibited the ERK signaling pathway, which, in turn, significantly reduced cardiomyocyte viability and contributed to mitochondrial dysfunction. Together, our results demonstrate that bevacizumab-mediated cardiotoxicity is associated with mitochondrial dysfunction, ER stress, and ERK pathway inactivation. These findings may provide potential treatment targets to attenuate myocardial injury during lung cancer immunotherapy.

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Section: Methodsmentioning

confidence: 99%

Bevacizumab‐Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity

Tian

Yue

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…ATG5 functions as an autophagy elongation protein in autophagosome formation and plays a crucial role in cancer (28)(29)(30). To identify the role of ATG5 in METTL3mediated autophagy, we first explored the relationship between METTL3 and ATG5.…”

Section: Mettl3 Promotes Autophagy and Resistance To Cisplatin By Tarmentioning

confidence: 99%

The m6A methyltransferase METTL3 regulates autophagy and sensitivity to cisplatin by targeting ATG5 in seminoma

Chen¹,

Xiang²,

Yin³

et al. 2021

Transl Androl Urol

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“…The activation of autophagy is needed for cell death induction during replicative crisis and therefore must be inhibited for cancer to be initiated. In ATG5-and ATG7-depleted cells, cytosolic DNA accumulates causing the activation of STING, STAT1 and associated ISG15 expression [93]. This STAT1-ISG15 axis promotes migration, invasion and proliferation of cells, suggesting that inhibition of autophagy can promote tumour-associated phenotypes through STING activation [93].…”

Section: Autophagy Regulates the Cgas-sting Pathwaymentioning

confidence: 99%

“…In ATG5-and ATG7-depleted cells, cytosolic DNA accumulates causing the activation of STING, STAT1 and associated ISG15 expression [93]. This STAT1-ISG15 axis promotes migration, invasion and proliferation of cells, suggesting that inhibition of autophagy can promote tumour-associated phenotypes through STING activation [93]. Thus, whilst STING-induced autophagy may inhibit the development of precancerous cells, autophagy inhibition may be utilised during tumorigenesis to activate STING and promote tumour phenotypes.…”

Section: Autophagy Regulates the Cgas-sting Pathwaymentioning

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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Deleting key autophagy elongation proteins induces acquirement of tumor-associated phenotypes via ISG15

Cited by 19 publications

References 65 publications

Bevacizumab‐Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity

Bevacizumab‐Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity

The m6A methyltransferase METTL3 regulates autophagy and sensitivity to cisplatin by targeting ATG5 in seminoma

Autophagy, the innate immune response and cancer

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