Beclin 1-mediated macroautophagy involves regulation of caspase-9 expression in cervical cancer HeLa cells

Wang, Zanhong; Xu, Li; Zhen-ling, Duan; Zeng, Linjuan; Yan, Naihong; Peng, Zhilan

doi:10.1016/j.ygyno.2007.05.034

Cited by 67 publications

(50 citation statements)

References 26 publications

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“…In 1999, Beclin1 was observed to be the key gene in the induction of autophagy, and it was the first gene that was identified to inhibit tumors through lysosome degradation (2). Studies have revealed that Beclin1 expression is decreased in cervical cancer (14), ovarian cancer (15) and cerebral tumors (16). Downregulation of Beclin1 expression significantly reduces autophagy in cancer cells (17,18).…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“…Beclin 1 is proposed to function as a tumour suppressor by promoting cellular macroautophagy and also may be an important 'molecular switch' to adjust autophagy and apoptosis in mammalian cells (Wang et al, 2007). The tumour-suppressing effect of Beclin 1 might be related to a role in regulating autophagic cell death.…”

Section: Discussionmentioning

confidence: 99%

The pivotal role of c-Jun NH2-terminal kinase-mediated Beclin 1 expression during anticancer agents-induced autophagy in cancer cells

et al. 2008

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“…In fact, overexpression of beclin 1, per se, is able to increase basal as well as induced autophagy in both normal and cancerous tissue and cells. 17,102,103 Thus, understanding the crosstalk between DDR and autophagy may be essential to understand how autophagy has either a positive or negative role in cell death induction after activation of DDR-induced autophagy. Recent advances in the field of transcription factors and effector proteins are addressing these questions and may aid in the understanding of how cells define their fate in this context.…”

Section: Parpmentioning

confidence: 99%

Autophagy and genomic integrity

et al. 2013

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DNA lesions, constantly produced by endogenous and exogenous sources, activate the DNA damage response (DDR), which involves detection, signaling and repair of the damage. Autophagy, a lysosome-dependent degradation pathway that is activated by stressful situations such as starvation and oxidative stress, regulates cell fate after DNA damage and also has a pivotal role in the maintenance of nuclear and mitochondrial genomic integrity. Here, we review important evidence regarding the role played by autophagy in preventing genomic instability and tumorigenesis, as well as in micronuclei degradation. Several pathways governing autophagy activation after DNA injury and the influence of autophagy upon the processing of genomic lesions are also discussed herein. In this line, the mechanisms by which several proteins participate in both DDR and autophagy, and the importance of this crosstalk in cancer and neurodegeneration will be presented in an integrated fashion. At last, we present a hypothetical model of the role played by autophagy in dictating cell fate after genotoxic stress.

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Beclin 1-mediated macroautophagy involves regulation of caspase-9 expression in cervical cancer HeLa cells

Cited by 67 publications

References 26 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

The pivotal role of c-Jun NH2-terminal kinase-mediated Beclin 1 expression during anticancer agents-induced autophagy in cancer cells

Autophagy and genomic integrity

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