Nuclear miR-30b-5p suppresses TFEB-mediated lysosomal biogenesis and autophagy

Guo, Huijie; Pu, M.; Tai, Yusi; Chen, Yuxiang; Lu, Henglei; Qiao, Junwen; Wang, Guanghui; Chen, Jing; Qi, Xinming; Huang, Ruimin; Tao, Zhouteng; Ren, Jin

doi:10.1038/s41418-020-0602-4

Cited by 42 publications

(27 citation statements)

References 52 publications

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“…The high abundance of miRNAs in the nucleus suggests their functional roles in transcriptional and post-transcriptional regulation in cellular homeostasis and human diseases. Recently, nuclear miR-30b-5p was reported to target coordinated lysosomal expression and regulation (CLEAR) elements and negatively regulate lysosomal biogenesis and autophagy in a transcription factor EB (TFEB)-dependent manner [43]. Furthermore, nuclear miR-320 up-regulates CD36 expression by directly activating transcription, whereas the inhibition of nuclear miR-320 could rescue cardiac dysfunction in diabetic mice [44,45].…”

Section: Nuclear Localizationmentioning

confidence: 99%

Subcellular Localization of miRNAs and Implications in Cellular Homeostasis

Jie

Feng

Huang

et al. 2021

Genes

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MicroRNAs (miRNAs) are thought to act as post-transcriptional regulators in the cytoplasm by either dampening translation or stimulating degradation of target mRNAs. With the increasing resolution and scope of RNA mapping, recent studies have revealed novel insights into the subcellular localization of miRNAs. Based on miRNA subcellular localization, unconventional functions and mechanisms at the transcriptional and post-transcriptional levels have been identified. This minireview provides an overview of the subcellular localization of miRNAs and the mechanisms by which they regulate transcription and cellular homeostasis in mammals, with a particular focus on the roles of phase-separated biomolecular condensates.

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Section: Nuclear Localizationmentioning

confidence: 99%

Subcellular Localization of miRNAs and Implications in Cellular Homeostasis

Jie

Feng

Huang

et al. 2021

Genes

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“…It is reported that miR-30b can inhibit autophagy [ 22 ]. Baicalein protected PD rats by mitochondrial autophagy.…”

Section: Resultsmentioning

confidence: 99%

“…miR-30b is reported to show the effect of inhibiting of autophagy [ 22 ]. It was found by our previous experiments that baicalein played a protective role through mitochondrial autophagy.…”

Section: Discussionmentioning

confidence: 99%

Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease

Chen

Peng

Gong

et al. 2021

Biochemistry Research International

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Parkinson’s disease (PD) is regarded as a severe neurodegenerative disorder. Baicalein is involved in the treatment of PD. This study explored the mechanism of baicalein in PD. The PD rat model was established using 6-hydroxydopamine. The neurologic score, dopamine (DA) content, apoptotic cells, and neuronal damage were evaluated after rats were treated with baicalein. Autophagy in PD rats was inhibited using 3-methyladenine (3-MA). The mitochondrial membrane potential (MMP) and autophagy-related proteins (LC3, P62) were detected. Next, agomiR-30b was transfected into PD rats. The targeting relation between miR-30b and NIX was predicted and verified. Then, sh-NIX was transfected into PD rats, and the effects of miR-30b and NIX on MMP, LC3, and P62 were assessed. When miR-30b was overexpressed using agomiR-30b, the NIX and BNIP3 levels were detected. Baicalein increased the neurological score and restored DA content, neurons, MMP, and mitochondrial autophagy protein levels. Baicalein inhibited miR-30b expression and miR-30b targeted NIX. miR-30b upregulation or NIX silencing reversed the effect of baicalein on MMP and mitochondrial autophagy. Baicalein upregulated NIX and BNIP3 expressions, while miR-30b overexpression inhibited NIX and BNIP3 expressions. In summary, baicalein mediated mitochondrial autophagy and restored neuronal activity by downregulating miR-30b and activating the NIX/BNIP3 pathway, thus protecting against PD.

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“…The time difference of gene and protein expression contribute to the confliction of downregulation of xenophagy gene (ULK1, ATG5 and ATG12) and increment of xenophagy protein expression (LC3) (Schwanhäusser et al, 2011). MiR-30b-5p was proven to be a nuclear miRNA that can transfer into the nucleus and inhibit the function of TFEB (Guo et al, 2020). TFEB is the master FIGURE 9 | Proposed mechanism of PA against intracellular H. pylori.…”

Section: Discussionmentioning

confidence: 99%

Clinical Strains of Helicobacter pylori With Strong Cell Invasiveness and the Protective Effect of Patchouli Alcohol by Improving miR-30b/C Mediated Xenophagy

Deng

Zhong

et al. 2021

Front. Pharmacol.

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Helicobacter pylori was classified by the World Health Organization as a class 1 carcinogen. The development of drug-resistant strains of this pathogen poses a serious threat to human health worldwide. The cell invasion of H. pylori activates xenophagy in gastric epithelial cells by mediating miR-30b/c, and the emergence of autophagosomes provides a niche that enables the survival of intracellular H. pylori and promotes its drug resistance. This study revealed that some clinical drug-resistant H. pylori strains present much stronger invasive ability than standard strains. Patchouli alcohol (PA), a tricyclic sesquiterpene from Pogostemon cablin (Blanco) Benth (Labiatae), showed reliable activity against intracellular H. pylori. The mechanisms appeared to involve the downregulation of miR-30c-3p/5p and miR-30b-5p, thereby upregulating xenophagy-related gene expression (ULK1, ATG5, ATG12, and ATG14) and enhancing xenophagy. PA also inhibited the nuclear transfection of miR-30b-5p induced by H. pylori, thereby enhancing transcription factor EB function and increasing lysosome activity. The finding of strongly invasive intracellular H. pylori has great implications for clinical treatment, and PA can act against invasive H. pylori based on the improvement of miR-30b/c mediated xenophagy. Taken together, the results demonstrate that PA have potential use as a candidate medication for intracellular drug-resistant H. pylori.

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Nuclear miR-30b-5p suppresses TFEB-mediated lysosomal biogenesis and autophagy

Cited by 42 publications

References 52 publications

Subcellular Localization of miRNAs and Implications in Cellular Homeostasis

Subcellular Localization of miRNAs and Implications in Cellular Homeostasis

Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease

Clinical Strains of Helicobacter pylori With Strong Cell Invasiveness and the Protective Effect of Patchouli Alcohol by Improving miR-30b/C Mediated Xenophagy

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