Beclin 1 deficiency is associated with increased hypoxia-induced angiogenesis

Lee, Seon-Jin; Kim, Hong-Pyo; Jin, Yang; Choi, Augustine M.K.; Ryter, Stefan W.

doi:10.4161/auto.7.8.15598

Cited by 112 publications

(82 citation statements)

References 49 publications

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“…Additionally, autophagy plays dual roles in tumor development (20). As a regulatory protein of autophagy, Beclin1 efficiently inhibits the development of tumors by inhibiting angiogenesis (21). Therefore, the present results provide experimental evidence for the use of Apelin-13 in the treatment of hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 61%

Apelin-13 induces autophagy in hepatoma HepG2 cells through ERK1/2 signaling pathway-dependent upregulation of Beclin1

Huang

Cao

et al. 2015

Oncology Letters

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Abstract. The aim of the present study was to investigate the effect of Apelin-13 on autophagy in hepatocellular carcinoma HepG2 cells and the underlying mechanism of the effect. The HepG2 cells were treated with Apelin-13 at a final concentration of 0.0001, 0.001, 0.01 and 0.1 µmol/l for 24 h. Cells were also treated with 10 µmol/l PD98059 for 24 h. The expression of the extracellular signal-regulated kinase (ERK)1/2, phosphorylated ERK1/2 (pERK1/2) and Beclin1 proteins were detected by western blot analysis. Beclin1 mRNA expression was also detected by reverse transcription-polymerase chain reaction. Autophagy was observed using fluorescence microscopy subsequent to monodansylcadaverine (MDC) staining. Following treatment with the various concentrations of Apelin-13, the expression of the ERK1/2 protein remained at a similar level, whereas the expression of pERK1/2 increased in a dose-dependent manner. Compared with the control group, the increase was significant (P<0.05). Similarly, Beclin1 expression was upregulated at the protein and mRNA levels by Apelin-13 treatment in a dose-dependent manner and was significantly increased compared with the control group. However, following treatment with the Apelin-13 inhibitor PD98059, the expression of pERK1/2, Beclin1 protein and Beclin1 mRNA were significantly decreased (P<0.05). In addition, Apelin-13 induced the autophagy of HepG2 cells in a dose-dependent manner, as revealed by MDC staining. PD98059 inhibited autophagy of HepG2 cells induced by Apelin-13. Therefore, Apelin-13 may promote autophagy in HepG2 cells by inducing the phosphorylation of ERK1/2 and upregulating the expression of Beclin1.

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Section: Discussionmentioning

confidence: 61%

Apelin-13 induces autophagy in hepatoma HepG2 cells through ERK1/2 signaling pathway-dependent upregulation of Beclin1

Huang

Cao

et al. 2015

Oncology Letters

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“…Conversely, overexpression of LC3B in vascular cells supressed mitogen and hypoxia-dependent proliferative responses in cultured vascular cells (91). Becn1 + /-endothelial cells also displayed enhanced proliferation in vitro in response to hypoxia relative to wild-type cells (90). These studies described a function of LC3B in regulating vascular cell responses to hypoxia, though the possibility that LC3B affects signaling pathways independent of autophagic regulation could not be excluded (91).…”

Section: Autophagy In Hypoxiamentioning

confidence: 81%

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Nakahira

Cloonan

Mizumura

et al. 2014

Antioxidants & Redox Signaling

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Significance: Autophagy is a fundamental cellular process that functions in the turnover of subcellular organelles and protein. Activation of autophagy may represent a cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Autophagy can increase survival during nutrient deficiency and play a multifunctional role in host defense, by promoting pathogen clearance and modulating innate and adaptive immune responses. Recent Advances: Autophagy has been described as an inducible response to oxidative stress. Once believed to represent a random process, recent studies have defined selective mechanisms for cargo assimilation into autophagosomes. Such mechanisms may provide for protein aggregate detoxification and mitochondrial homeostasis during oxidative stress. Although long studied as a cellular phenomenon, recent advances implicate autophagy as a component of human diseases. Altered autophagy phenotypes have been observed in various human diseases, including lung diseases such as chronic obstructive lung disease, cystic fibrosis, pulmonary hypertension, and idiopathic pulmonary fibrosis. Critical Issues: Although autophagy can represent a pro-survival process, in particular, during nutrient starvation, its role in disease pathogenesis may be multifunctional and complex. The relationship of autophagy to programmed cell death pathways is incompletely defined and varies with model system. Future Directions: Activation or inhibition of autophagy may be used to alter the progression of human diseases. Further resolution of the mechanisms by which autophagy impacts the initiation and progression of diseases may lead to the development of therapeutics specifically targeting this pathway. Antioxid. Redox Signal. 20,

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“…Indeed, a deficiency in BECN1, an initiator of autophagy, is associated with increased hypoxia-induced angiogenesis. 48 In contrast, BECN1 overexpression inhibits the proliferation, invasion, and migration of cervical cancer cells. E and F), MDA-MB-231 cells were pretreated with or without rapamycin for 3 h before exposure to 2A-cM.…”

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confidence: 99%

Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells

et al. 2014

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Beclin 1 deficiency is associated with increased hypoxia-induced angiogenesis

Cited by 112 publications

References 49 publications

Apelin-13 induces autophagy in hepatoma HepG2 cells through ERK1/2 signaling pathway-dependent upregulation of Beclin1

Apelin-13 induces autophagy in hepatoma HepG2 cells through ERK1/2 signaling pathway-dependent upregulation of Beclin1

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells

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