MiR-20a and miR-106b negatively regulate autophagy induced by leucine deprivation via suppression of ULK1 expression in C2C12 myoblasts

Wu, Hao; Wang, Fengli; Hu, Songtao; Yin, Cong; Li, Xiao; Song, Zhao; Wang, Junjun; Yan, Xianghua

doi:10.1016/j.cellsig.2012.07.001

Cited by 128 publications

(95 citation statements)

References 45 publications

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“…Previous studies have demonstrated that miR-24 (21), and the other upregulated miRNAs identified in the present study [miR-17 (22), miR-20a (23,24), miR-25 (25), miR-30d (26,27) and miR-451 (28)], are associated with autophagy. These miRNAs serve a role in inhibiting autophagy, downregulating the expression of target genes (Table IV).…”

Section: Discussionsupporting

confidence: 68%

Serum microRNA expression profiling in patients with multiple system atrophy

Kume

Iwama

Deguchi

et al. 2017

Journal of the Neurological Sciences

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Section: Discussionsupporting

confidence: 68%

Serum microRNA expression profiling in patients with multiple system atrophy

Kume

Iwama

Deguchi

et al. 2017

Journal of the Neurological Sciences

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“…Numerous miRNAs, such as miR-20a, miR-30a, miR-34a, miR101, miR-106b, and miR-375, regulate autophagy by suppressing autophagy-related proteins [4,9,37]. Wu et al reported that miR-20a and miR-106b negatively regulate starvation-induced autophagy by suppressing ULK1 in C2C12 myoblasts [37].…”

Section: Discussionmentioning

confidence: 99%

MiR-20a-5p mediates hypoxia-induced autophagy by targeting ATG16L1 in ischemic kidney injury

et al. 2015

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“…For example, STAT3 upregulates MIR17HG (miR-17-92 cluster host gene [non-protein coding]) through a highly conserved STAT3 binding site in the promoter region, 52 and members of the MIR17HG cluster have been reported to target the autophagy-related genes ULK1, BECN1, and BCL2L11. [53][54][55] Several miRNAs that have been transcriptionally modulated by STAT3 and have been reported to target autophagy pathways are summarized in Table 2. 26,52-64 However, the role of miRNAs in the regulation of STAT3-mediated autophagy has not been well established, and this need to be further investigated.…”

Section: Stat3 In Autophagymentioning

confidence: 99%

The role of STAT3 in autophagy

et al. 2015

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Abbreviations: ALK, anaplastic lymphoma receptor tyrosine kinase; ATF4, activating transcription factor 4; BNIP3, BCL2/adenovirus E1B 19kDa interacting protein 3; CNTF, ciliary neurotrophic factor; COX8, cytochrome c oxidase subunit VIII; ConA, concanavalin A; CTSB, cathepsin B; CTSL, cathepsin L; CuB, cucurbitacin B; CYCS, cytochrome c, somatic; EGF, epidermal growth factor; EIF2A, eukaryotic initiation factor 2A, 65kDa; EIF2AK2, eukaryotic translation initiation factor 2-a kinase 2; ER, endoplasmic reticulum; ETC, electron transport chain; FOXO1/3, forkhead box O1/3; HDAC3, histone deacetylase 3; HIF1A, hypoxia inducible factor 1, a subunit (basic helix-loop-helix transcription factor); IL6, interleukin 6; IMM, inner mitochondrial membrane; KDR, kinase insert domain receptor; LMP, lysosomal membrane permeabilization; MAPK1, mitogen-activated protein kinase 1; MAP1LC3A, microtubule-associated protein 1 light chain 3 a; miRNA, microRNA; mitoSTAT3, mitochondrial STAT3; MLS, mitochondrial localization sequence; MMP14, matrix metallopeptidase 14 (membrane-inserted); NDUFA13, NADH dehydrogenase (ubiquinone) 1 a subcomplex, 13; NES, nuclear export signal; NFKB1, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1; NLS, nuclear localization signal; PDGFRB, platelet-derived growth factor receptor, b polypeptide; PRKAA2, protein kinase, AMP-activated, a 2 catalytic subunit; PTPN2, protein tyrosine phosphatase, non-receptor type 2; PTPN6, protein tyrosine phosphatase, non-receptor type 6; PTPN11, protein tyrosine phosphatase, non-receptor type 11; ROS, reactive oxygen species; RTK, receptor tyrosine kinases; SH2, src homology 2; STAT3, signal transducer and activator of transcription 3 (acute-phase response factor); VHL, von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase; XPO1, exportin 1.Autophagy is an evolutionarily conserved process in eukaryotes that eliminates harmful components and maintains cellular homeostasis in response to a series of extracellular insults. However, these insults may trigger the downstream signaling of another prominent stress responsive pathway, the STAT3 signaling pathway, which has been implicated in multiple aspects of the autophagic process. Recent reports further indicate that different subcellular localization patterns of STAT3 affect autophagy in various ways. For example, nuclear STAT3 fine-tunes autophagy via the transcriptional regulation of several autophagy-related genes such as BCL2 family members, BECN1, PIK3C3, CTSB, CTSL, PIK3R1, HIF1A, BNIP3, and microRNAs with targets of autophagy modulators. Cytoplasmic STAT3 constitutively inhibits autophagy by sequestering EIF2AK2 as well as by interacting with other autophagy-related signaling molecules such as FOXO1 and FOXO3. Additionally, the mitochondrial translocation of STAT3 suppresses autophagy induced by oxidative stress and may effectively preserve mitochondria from being degraded by mitophagy. Understanding the role of STAT3 signaling in the regulation of autophagy may provide insight into the cla...

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MiR-20a and miR-106b negatively regulate autophagy induced by leucine deprivation via suppression of ULK1 expression in C2C12 myoblasts

Cited by 128 publications

References 45 publications

Serum microRNA expression profiling in patients with multiple system atrophy

Serum microRNA expression profiling in patients with multiple system atrophy

MiR-20a-5p mediates hypoxia-induced autophagy by targeting ATG16L1 in ischemic kidney injury

The role of STAT3 in autophagy

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