LETM1 Knockdown Promotes Autophagy and Apoptosis Through AMP-Activated Protein Kinase Phosphorylation-Mediated Beclin-1/Bcl-2 Complex Dissociation in Hepatocellular Carcinoma

Zhou, Baoyong; Yang, Chengliang; Xiong, Ye; Shi, Zhengrong; Xiao, Heng; Wei, Xufu; Jiang, Ning; Wu, Zhongjun

doi:10.3389/fonc.2020.606790

Cited by 10 publications

(7 citation statements)

References 36 publications

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“…However, the combination of Beclin-1 to Bcl-2 generally results in autophagy in an inhibited state. Unbinding of Bcl-2 from Beclin-1 may be an essential requirement for autophagy upregulation [ 33 , 34 ].…”

Section: Introductionmentioning

confidence: 99%

Autophagy in hepatic ischemia–reperfusion injury

Mao

Yuan

et al. 2023

Cell Death Discov.

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Hepatic ischemia–reperfusion injury (HIRI) is a major complication of liver resection or liver transplantation that can seriously affect patient’s prognosis. There is currently no definitive and effective treatment strategy for HIRI. Autophagy is an intracellular self-digestion pathway initiated to remove damaged organelles and proteins, which maintains cell survival, differentiation, and homeostasis. Recent studies have shown that autophagy is involved in the regulation of HIRI. Numerous drugs and treatments can change the outcome of HIRI by controlling the pathways of autophagy. This review mainly discusses the occurrence and development of autophagy, the selection of experimental models for HIRI, and the specific regulatory pathways of autophagy in HIRI. Autophagy has considerable potential in the treatment of HIRI.

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Section: Introductionmentioning

confidence: 99%

Autophagy in hepatic ischemia–reperfusion injury

Mao

Yuan

et al. 2023

Cell Death Discov.

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“…The p62 protein can directly bind to LC3B-II during the formation of autophagosomes to eliminate the ubiquitinated misfolded proteins, and thus has also been frequently used to monitor the autophagic activities [45]. On the other hand, Bcl-2 functions as an inhibitor of Beclin-1mediated autophagy by directly binding to Beclin-1 [46]. As shown in Figure 7, compared with the mock group, exposure to NaIO 3 resulted in decreased Bcl-2 and increased levels of Beclin-1, LC3B-II, and p62.…”

Section: Quercetin Influenced the Expression Of Autophagic Proteinsmentioning

confidence: 99%

Quercetin Alleviates the Accumulation of Superoxide in Sodium Iodate-Induced Retinal Autophagy by Regulating Mitochondrial Reactive Oxygen Species Homeostasis through Enhanced Deacetyl-SOD2 via the Nrf2-PGC-1α-Sirt1 Pathway

et al. 2021

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Oxidative damage of retinal pigment epithelium (RPE) cells plays an important role in the pathogenesis of blindness-related diseases, such as age-related macular degeneration (AMD). Quercetin, a bioactive flavonoid compound, has been shown to have a protective effect against oxidative stress-induced cell apoptosis and inflammation in RPE cells; however, the detailed mechanism underlying this protective effect is unclear. Therefore, the aim of this study was to investigate the regulatory mechanism of quercetin in a sodium iodate (NaIO3)-induced retinal damage. The clinical features of the mice, the production of oxidative stress, and the activity of autophagy and mitochondrial biogenesis were examined. In the mouse model, NaIO3 treatment caused changes in the retinal structure and reduced pupil constriction, and quercetin treatment reversed the oxidative stress-related pathology by decreasing the level of superoxide dismutase 2 (SOD2) while enhancing the serum levels of catalase and glutathione. The increased level of reactive oxygen species in the NaIO3-treated ARPE19 cells was improved by treatment with quercetin, accompanied by a reduction in autophagy and mitochondrial biogenesis. Our findings indicated that the effects of quercetin on regulating the generation of mtROS were dependent on increased levels of deacetyl-SOD2 through the Nrf2-PGC-1α-Sirt1 signaling pathway. These results demonstrated that quercetin may have potential therapeutic efficacy for the treatment of AMD through the regulation of mtROS homeostasis.

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“…LETM1 expression is increased in many cancers [ 83 , 205 ]. In most cases, LETM1 appears to be pro-tumorigenic [ 206 , 207 ]. The open questions surrounding the substrate specificity and stoichiometry of LETM1 ( Section 2.2 ) preclude understanding of roles of LETM1 mediated transport in cancer.…”

Section: Dysregulation Of Mitochondrial Ion Channels and Transporters In Cancermentioning

confidence: 99%

The Interplay between Dysregulated Ion Transport and Mitochondrial Architecture as a Dangerous Liaison in Cancer

Pedersen

Flinck

Pardo

2021

IJMS

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Transport of ions and nutrients is a core mitochondrial function, without which there would be no mitochondrial metabolism and ATP production. Both ion homeostasis and mitochondrial phenotype undergo pervasive changes during cancer development, and both play key roles in driving the malignancy. However, the link between these events has been largely ignored. This review comprehensively summarizes and critically discusses the role of the reciprocal relationship between ion transport and mitochondria in crucial cellular functions, including metabolism, signaling, and cell fate decisions. We focus on Ca2+, H+, and K+, which play essential and highly interconnected roles in mitochondrial function and are profoundly dysregulated in cancer. We describe the transport and roles of these ions in normal mitochondria, summarize the changes occurring during cancer development, and discuss how they might impact tumorigenesis.

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LETM1 Knockdown Promotes Autophagy and Apoptosis Through AMP-Activated Protein Kinase Phosphorylation-Mediated Beclin-1/Bcl-2 Complex Dissociation in Hepatocellular Carcinoma

Cited by 10 publications

References 36 publications

Autophagy in hepatic ischemia–reperfusion injury

Autophagy in hepatic ischemia–reperfusion injury

Quercetin Alleviates the Accumulation of Superoxide in Sodium Iodate-Induced Retinal Autophagy by Regulating Mitochondrial Reactive Oxygen Species Homeostasis through Enhanced Deacetyl-SOD2 via the Nrf2-PGC-1α-Sirt1 Pathway

The Interplay between Dysregulated Ion Transport and Mitochondrial Architecture as a Dangerous Liaison in Cancer

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