YY1-<i>MIR372</i>-SQSTM1 regulatory axis in autophagy

Feng, Lifeng; Ma, Yanning; Sun, Jie; Shen, Qi; Liu, Leiming; Lu, Haiqi; Wang, Faliang; Yue, Yongfang; Li, Jiaqiu; Zhang, Shenjie; Lin, Xiaoying; Chu, Jue; Han, Weidong; Wang, Xian; Jin, Hongchuan

doi:10.4161/auto.29486

Cited by 62 publications

(51 citation statements)

References 43 publications

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“…Feng et al (2014) examined the relationship between autophagy activation and human carcinogenesis. They demonstrated that there was an epigenetic regulation, namely, i) knockdown of YY1 inhibited cell viability and autophagy flux through downregulation of SQSTM1 (sequestosome 1) ii) the regulation of SQSTM1 is epigenetically modulated by the transcription of miR372, which targets directly SQSTM1 and iii) stimulation of YY1 promotes SQSTM1 expression and suppresses miR372 expression, inhibiting the activation of autophagy.…”

Section: Yin Yang 1 and Autophagymentioning

confidence: 99%

Prognostic significance of YY1 protein expression and mRNA levels by bioinformatics analysis in human cancers: A therapeutic target

Bonavida

Kaufhold

2015

Pharmacology & Therapeutics

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Section: Yin Yang 1 and Autophagymentioning

confidence: 99%

Prognostic significance of YY1 protein expression and mRNA levels by bioinformatics analysis in human cancers: A therapeutic target

Bonavida

Kaufhold

2015

Pharmacology & Therapeutics

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“…As a highly conserved transcription factor, YY1 has been reported as a meaningful autophagy regulator in recent years . Under nutrient starvation, YY1 expression elevates to activate autophagy by inhibiting miR‐372 in breast cancer . Here, we find that YY1 is a cofactor of TFEB, and combined expression of YY1 and TFEB is additive towards autophagy and lysosome biogenesis.…”

Section: Discussionmentioning

confidence: 65%

“…YY1 functions as an activator or a repressor depending on its spatial and temporal context . It is noteworthy that recent studies demonstrate YY1 modulates autophagy in cancer cells through YY1‐miRNA regulatory circuits . Moreover, autophagy flux was inhibited in breast cancer cells with YY1 knockdown, implying the essential roles of YY1 in modulating autophagy .…”

Section: Introductionmentioning

confidence: 99%

YY1 cooperates with TFEB to regulate autophagy and lysosomal biogenesis in melanoma

Ren

Yao

et al. 2019

Molecular Carcinogenesis

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Autophagy is a self‐proteolytic process that degrades intracellular material to maintain cellular homeostasis. Transcription factor EB (TFEB) is the master activator that regulates the transcription of genes involved in autophagy and lysosomal biogenesis. However, the cotranscriptional factors of TFEB are rarely identified. Here, we found that Yin Yang 1 (YY1) regulated autophagy and lysosome biogenesis in melanoma cells. YY1 cooperates with TFEB to regulate autophagy through controlling the transcription of autophagy and lysosome biogenesis related genes. Moreover, suppression of YY1 enhanced the antitumor efficiency of vemurafenib both in vitro and in vivo. Collectively, these studies identify YY1 as a novel cotranscription factor of TFEB in regulating autophagy and lysosomal functions and suggest YY1 could be a therapeutic target in cancer treatment.

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“…UBC-LC3-GFP lentivirus was purchased from Shanghai Genechem Co., Ltd. (Shanghai, China) (24). Lentivirus infection was according to the manufacturer (Shanghai GeneChem Co, Ltd.) at a final concentration of 100–200 multiplicity of infection (MOI).…”

Section: Methodsmentioning

confidence: 99%

Inhibiting PLK1 induces autophagy of acute myeloid leukemia cells via mammalian target of rapamycin pathway dephosphorylation

Tao

et al. 2017

Oncology Reports

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Decreased autophagy is accompanied by the development of a myeloproliferative state or acute myeloid leukemia (AML). AML cells are often sensitive to autophagy-inducing stimuli, prompting the idea that targeting autophagy can be useful in AML cytotoxic therapy. AML NB4 cells overexpressing microtubule-associated protein 1 light chain 3-green fluorescent protein were screened with 69 inhibitors to analyze autophagy activity. AML cells were treated with the polo-like kinase 1 (PLK1) inhibitors RO3280 and BI2536 before autophagy analysis. Cleaved LC3 (LC3-II) and the phosphorylation of mammalian target of rapamycin (mTOR), adenosine monophosphate-activated protein kinase, and Unc-51-like kinase 1 during autophagy was detected with western blotting. Autophagosomes were detected using transmission electron microscopy. Several inhibitors had promising autophagy inducer effects: BI2536, MLN0905, SK1-I, SBE13 HCL and RO3280. Moreover, these inhibitors all targeted PLK1. Autophagy activity was increased in the NB4 cells treated with RO3280 and BI2536. Inhibition of PLK1 expression in NB4, K562 and HL-60 leukemia cells with RNA interference increased LC3-II and autophagy activity. The phosphorylation of mTOR was reduced significantly in NB4 cells treated with RO3280 and BI2536, and was also reduced significantly when PLK1 expression was downregulated in the NB4, K562 and HL-60 cells. We demonstrate that PLK1 inhibition induces AML cell autophagy and that it results in mTOR dephosphorylation. These results may provide new insights into the molecular mechanism of PLK1 in regulating autophagy.

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YY1-MIR372-SQSTM1 regulatory axis in autophagy

Cited by 62 publications

References 43 publications

Prognostic significance of YY1 protein expression and mRNA levels by bioinformatics analysis in human cancers: A therapeutic target

Prognostic significance of YY1 protein expression and mRNA levels by bioinformatics analysis in human cancers: A therapeutic target

YY1 cooperates with TFEB to regulate autophagy and lysosomal biogenesis in melanoma

Inhibiting PLK1 induces autophagy of acute myeloid leukemia cells via mammalian target of rapamycin pathway dephosphorylation

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