MicroRNA-125b-5p improves pancreatic β-cell function through inhibiting JNK signaling pathway by targeting DACT1 in mice with type 2 diabetes mellitus

Yu, Chengyong; Yang, Chun-Yun; Rui, Zhilian

doi:10.1016/j.lfs.2019.01.031

Cited by 44 publications

(29 citation statements)

References 45 publications

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“…24 Besides, the ERK and AKT pathway are two key signalling pathways involved in the progression of various tumours and is associated with cancer malignant proliferation. 25,26 Members of the MMP family degrade extracellular matrix and cell surface proteins, thus playing an important role in cancer cell invasion. A high level of MMP-7 predicts poor survival in patients at an advanced stage of lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Retracted: KIF20A silence inhibits the migration, invasion and proliferation of non‐small cell lung cancer and regulates the JNK pathway

Xie

Gao

et al. 2019

Clin Exp Pharma Physio

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Lung cancer is the most frequently-occurring tumour and the leading cause of cancer-related death worldwide. 1 As the predominant type of lung cancer, non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. 2 More than 90% of NSCLC patients are triggered by tumour progression, especially distant metastasis, 3 and metastasis has been a critical contributor to mortality rate. 4 Therefore, exploring potential therapeutic targets of NSCLC metastasis is required for more effective clinical therapies. The kinesin family (KIF) contains 14 super families ranging from kinesin-1 to kinesin-14. Kinesin family member 20A (KIF20A), locates on chromosome 5q31.2 and belongs to kinesin family-6, sharing a highly conserved motor domain with other kinesin family members. 5 KIF20A was up-regulated in malignant tumours but barely expressed in normal organs except the testis and thymus. 6 In 2005, for the first

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Section: Discussionmentioning

confidence: 99%

Retracted: KIF20A silence inhibits the migration, invasion and proliferation of non‐small cell lung cancer and regulates the JNK pathway

Xie

Gao

et al. 2019

Clin Exp Pharma Physio

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“…DEGs in GO terms and pathways might be linked with advancement of obesity associated type 2 diabetes mellitus. ERBB2 [36], DACT1 [37], ARAP1 [38], MYH9 [39], INPPL1 [40], SARM1 [41], NOTCH1 [42], ROBO1 [43], MAPK8IP1 [44], ANK1 [45], SARM1 [46], SREBF2 [47], SIK1 [48], PASK (PAS domain containing serine/threonine kinase) [49], NOS2 [50], OAS3 [51], KL (klotho) [52], PECAM1 [53], S100A12 [54], S100P [55], BATF3 [56], PLEK (pleckstrin) [57], ALOX5 [58], ARG1 [59], CXCL8 [60], CXCR1 [61], PTAFR (platelet activating factor receptor) [62], PYGL (glycogen phosphorylase L) [63], TCF4 [64], CAMP (cathelicidin antimicrobial peptide) [65], RUNX2 [66], PLA2G2A [67], GCG (glucagon) [68], RARRES2 [69] and HAP1 [70] were involved in the genesis of type 2 diabetes mellitus. Recent studies have reported that ACHE (acetylcholinesterase) [71], FGFR3 [72], VLDLR (very low density lipoprotein receptor) [73], SHC1 [74], HDAC6 [75], CHRNA2 [76], CASR (calcium sensing receptor) [77], ELK1 [78], TYK2 [79], CIITA (class II major histocompatibility complex transactivator) [80], ZAP70 [81], GPT (glutamic--pyruvic transaminase) [82], CHI3L1 [83], AIF1 [84], MMP9 [85], ITGB2 [86], CFD (complement factor D) [87], C3AR1 [88], LGALS1 [89], CD14 [90], TIMP1 [91], TLR2 [92], LTF (lactotransferrin) [93], BRCA2 [94] and IGFBP3 [95] promotes the development of obesity.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics Analysis of Key Genes and Pathways for Obesity Associated Type 2 Diabetes Mellitus as a Therapeutic Target

Vastrad¹,

Tengli

Vastrad³

et al. 2020

Preprint

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Obesity associated type 2 diabetes mellitus is one of the most common metabolic disorder worldwide. The prognosis of obesity associated type 2 diabetes mellitus patients has remained poor, though considerable efforts have been made to improve the treatment of this metabolic disorder. Therefore, identifying significant differentially expressed genes (DEGs) associated in metabolic disorder advancement and exploiting them as new biomarkers or potential therapeutic targets for metabolic disorder is highly valuable. Differentially expressed genes (DEGs) were screened out from gene expression omnibus (GEO) dataset (GSE132831) and subjected to GO and REACTOME pathway enrichment analyses. The protein - protein interactions network, module analysis, target gene - miRNA regulatory network and target gene - TF regulatory network were constructed, and the top ten hub genes were selected. The relative expression of hub genes was detected in RT-PCR. Furthermore, diagnostic value of hub genes in obesity associated type 2 diabetes mellitus patients was investigated using the receiver operating characteristic (ROC) analysis. Small molecules were predicted for obesity associated type 2 diabetes mellitus by using molecular docking studies. A total of 872 DEGs, including 439 up regulated genes and 432 down regulated genes were observed. Second, functional enrichment analysis showed that these DEGs are mainly involved in the axon guidance, neutrophil degranulation, plasma membrane bounded cell projection organization and cell activation. The top ten hub genes (MYH9, FLNA, DCTN1, CLTC, ERBB2, TCF4, VIM, LRRK2, IFI16 and CAV1) could be utilized as potential diagnostic indicators for obesity associated type 2 diabetes mellitus. The hub genes were validated in obesity associated type 2 diabetes mellitus. This investigation found effective and reliable molecular biomarkers for diagnosis and prognosis by integrated bioinformatics analysis, suggesting new and key therapeutic targets for obesity associated type 2 diabetes mellitus.

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“…The total protein of tissues or cells was extracted by using phenylmethylsulfonyl fluoride and protease inhibitors. The supernatant was extracted after tissues or cells were allowed to Establishment of a rat model of type 2 diabetes mellitus 15 In this substudy, 88 male Wistar rats (weighing 180-220 g, aged 4-6 weeks) were selected. The rats were housed in specific pathogen-free cages, and the surrounding environment was comprised of sterile, dry, constant temperature conditions, with water that had been disinfected with in high temperature conditions and food that had been disinfected with ultraviolet light.…”

Section: Western Blot Analysismentioning

confidence: 99%

Micro‐ribonucleic acid‐23a‐3p prevents the onset of type 2 diabetes mellitus by suppressing the activation of nucleotide‐binding oligomerization‐like receptor family pyrin domain containing 3 inflammatory bodies‐caused pyroptosis through negatively regulating NIMA‐related kinase 7

Chang

Cheng

et al. 2020

J of Diabetes Invest

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Aims/Introduction Micro‐ribonucleic acids (miRNAs) possess crucial functions in governing metabolisms associated with type 2 diabetes mellitus. This study aimed to investigate the role of miR‐23a‐3p in pyroptosis caused by nucleotide‐binding oligomerization‐like receptor family pyrin domain containing 3 (NLRP3) inflammatory body activation, thereby reducing the occurrence of type 2 diabetes mellitus. Materials and Methods miR‐23a‐3p and NIMA‐related kinase 7 (NEK7) expression in type 2 diabetes mellitus patients and rat models was examined. Dual‐luciferase reporter gene experiments were used to verify the targeting relationship between miR‐23a‐3p and NEK7. Bone marrow‐derived macrophages were transfected with miR‐23a‐3p mimic, miR‐23a‐3p inhibitor or short hairpin NEK7 and were treated with a specific activator of NLRP3 inflammatory body (lipopolysaccharide + adenosine‐5′‐triphosphate) to evaluate expression of NEK7, miR‐23a‐3p, gasdermin D p30, pro‐caspase‐1 and caspase‐1 in cells, and interleukin‐1β and tumor necrosis factor‐α in supernatant. Type 2 diabetes mellitus rat models were used to observe the influences of miR‐23a‐3p, NEK7 and NLRP3 inflammatory body on pyroptosis and type 2 diabetes mellitus in vivo. Results NEK7 was overexpressed, whereas miR‐23a‐3p was underexpressed in patients and rat models with type 2 diabetes mellitus. NEK7 was a target gene of miR‐23a‐3p. After the addition of lipopolysaccharide + adenosine‐5′‐triphosphate in bone marrow‐derived macrophages, the expression of miR‐23a‐3p subsequently declined. Furthermore, the addition of lipopolysaccharide + adenosine‐5′‐triphosphate elevated NEK7, NLRP3, pro‐caspase‐1, cle‐caspase‐1 and gasdermin D p30 expressions in bone marrow‐derived macrophages, and enhanced levels of interleukin‐1β and tumor necrosis factor‐α in the supernatant, accompanied with conspicuous cell pyroptosis, which was reversed after miR‐23a‐3p overexpression and NEK7 silencing. miR‐23a‐3p overexpression alleviated liver and kidney damage in type 2 diabetes mellitus rats, and reduced NLRP3‐induced pyroptosis. Conclusions Targeting NEK7 by miR‐23a‐3p could reduce NLRP3‐induced pyroptosis, and assuage liver and kidney injuries in type 2 diabetes mellitus rats.

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MicroRNA-125b-5p improves pancreatic β-cell function through inhibiting JNK signaling pathway by targeting DACT1 in mice with type 2 diabetes mellitus

Cited by 44 publications

References 45 publications

Retracted: KIF20A silence inhibits the migration, invasion and proliferation of non‐small cell lung cancer and regulates the JNK pathway

Retracted: KIF20A silence inhibits the migration, invasion and proliferation of non‐small cell lung cancer and regulates the JNK pathway

Bioinformatics Analysis of Key Genes and Pathways for Obesity Associated Type 2 Diabetes Mellitus as a Therapeutic Target

Micro‐ribonucleic acid‐23a‐3p prevents the onset of type 2 diabetes mellitus by suppressing the activation of nucleotide‐binding oligomerization‐like receptor family pyrin domain containing 3 inflammatory bodies‐caused pyroptosis through negatively regulating NIMA‐related kinase 7

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