<i>Retracted</i>: Effects of microRNA‐494 on proliferation, migration, invasion, and apoptosis of medulloblastoma cells by mediating <i>c‐myc</i> through the p38 MAPK signaling pathway

Xu, Xiaofei; Zhang, Si-Jin; Hu, Qibo; Song, Xingyu; Pan, Wei

doi:10.1002/jcb.27559

Cited by 17 publications

(11 citation statements)

References 39 publications

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“…Luckily, through preliminary data mining, we discovered that Myc has a close relationship with MAPK signaling pathway. More importantly, several studies uncovered that Myc expression was positively related to MAPK signaling pathway in asthma airway remodeling [34], osteoarthritis [35], and some tumors [36,37]. In steps with the previous, we discovered that depletion of Myc in LPS model can block the expression of p-P38 MAPK and p-JNK.…”

Section: Discussionsupporting

confidence: 72%

Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway

Huang

Zhang

et al. 2020

Bioscience Reports

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Background: Genistein is widely used as a pharmacological compound as well as a food additive. However, the pharmaceutical effects of Genistein on myocarditis and its potential mechanisms have not been studied in detail. Methods: H9c2 cells were continuously stimulated by lipopolysaccharide (LPS) for 12 h to simulate the in vitro model of myocarditis injury. DrugBank, String, and GEO dataset were used to investigate specific genes that interacting with Genistein. KEGG and GO enrichment analysis were employed to explore Myc-related signaling pathways. Biological behaviors of H9c2 cells were observed with the support of cell counting kit-8, MTT and flow cytometry. Expression levels of cytokines including TNF-α and ILs were evaluated by enzyme-linked immunosorbent assay. Western blot was applied to detect the expression of Myc and MAPK pathway related proteins. Results: Genistein alleviated the damage of H9c2 cells subjected to LPS from the perspective of elevating cells growth ability, and inhibiting cells apoptosis and inflammatory response. Through bioinformatics analysis, we identified Myc as the potential target of Genistein in myocarditis, and MAPK as the signaling pathway. Significantly, Myc was highly up-regulated in myocarditis samples. More importantly, by performing biological experiments, we discovered that Genistein relieved H9c2 cells apoptosis and inflammatory reaction which caused by LPS stimulation through inhibiting Myc expression. Additionally, the marked augmentation of p-P38 MAPK and p-JNK expression in LPS-induced cardiomyocyte model were blocked by Genistein and si-Myc. Conclusions: Our research revealed that Myc mediated the protective effects of Genistein on H9c2 cells damage caused by LPS partly through modulation of MAPK/JNK signaling pathway.

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Section: Discussionsupporting

confidence: 72%

Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway

Huang

Zhang

et al. 2020

Bioscience Reports

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“…Among the significant findings that summarized in our study, one of them suggested that miR-494 was down-regulated in hippocampal tissues of rats with Ep. Similar to this finding, the degradation of miR-494 has been verified in medulloblastoma tissues [11]. Cheng et al have found that the expression of miR-494 was repressed in cervical cancer [27].…”

Section: Discussionsupporting

confidence: 66%

“…miR-494 is situated at chromosome 14q32.31 [8] and has been revealed to be downregulated in temporal cortex of patients with mesial temporal lobe epilepsy (mTLE) [9]. Its mechanism functions have also been demonstrated in other neurological diseases, such as glioblastoma [10] and medulloblastoma [11]. Moreover, receptor-interacting protein kinase 1 (RIPK1) is a member of a serine-threonine kinase family that transfers inflammatory and cell death signals after death receptor ligation, activation of pattern recognition receptors, as well as DNA injury [12].…”

Section: Introductionmentioning

confidence: 99%

Overexpressed microRNA-494 represses RIPK1 to attenuate hippocampal neuron injury in epilepsy rats by inactivating the NF-κB signaling pathway

Qian

et al. 2020

Cell Cycle

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Objective: The effects of microRNAs (miRNAs) have been identified in epilepsy (Ep) in recent years, our research was focused on the functions of miR-494 in Ep and its inner mechanisms. Methods: The Ep modeled rats induced by lithium chloride-pilocarpine were treated with agomir-miR-494 or RIPK1-siRNA. The pathology of rat hippocampal tissues was observed. Expression of miR-494, receptor-interacting protein kinase 1 (RIPK1) and nuclear factor-kappaB (NF-κB) p65 was assessed by RT-qPCR and Western blot analysis. The hippocampal neurons of epileptic rats were successfully modeled, which were transfected with miR-494 mimics or RIPK1-siRNA to determine neurons' proliferation ability and cell apoptosis. The target relation between miR-494 and RIPK1 was measured by bioinformatics website and dual luciferase gene reporter assay. Results: The expression of miR-494 was reduced, while the expression of RIPK1 and NF-κB p65 was amplified in hippocampus of Ep rats. Elevated miR-494 repressed the expression of RIPK1 to ameliorate the hippocampal neuron injury, accelerate neuronal proliferation, and restrain neuronal apoptosis via inactivating the NF-κB signaling pathway, causing a deceleration of Ep development. Furthermore, amplified RIPK1 was able to reverse the amelioration of neuronal injury in Ep rats which was contributed by upregulated miR-494. Conclusion:We found in this study that elevated miR-494 repressed RIPK1, causing an inactivation of the NF-κB signaling pathway and acceleration of cell proliferation, and suppression of apoptosis of hippocampal neurons in Ep rats, thereby attenuating the neuron injury and Ep development. Our research may provide novel targets for the therapy of Ep.

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“…BDNF participates in the classical MAP kinase pathway by binding to its tyrosine kinase receptor TrkB, leading to cell proliferation and differentiation [ 21 ]. Downregulated c-myc could inactivate the p38 MAPK pathway and suppress cell proliferation and migration [ 22 ], suggesting that the upregulated c-myc observed in our study may induce these responses. DUSP is a group of dual-specificity phosphatases that are closely related to MAPK and mostly negatively regulate their function.…”

Section: Discussionmentioning

confidence: 97%

Changing Expression Profiles and Inclination to Competing Endogenous RNA Networks on MAPK Signaling Pathways of Human Adipose-Derived Stem Cells in a Direct Current Electric Field

Jin

Zhang

Bian

et al. 2020

BioMed Research International

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Adipose-derived stem cells (ADSCs) are an abundant cell source and provide an easy way to harvest mesenchymal stem cells, which are the focus of considerable attention in regenerative medicine. Electric fields (EF) play roles in many biological events and have been reported to promote cell proliferation, migration, and differentiation. In this study, ADSCs were treated with a direct current electric field (DCEF) of either 0 (control group) or 300 mV/mm (EF group) for six hours. RNA screening and analysis revealed that 66, 164, 26, and 1310 circRNAs, lncRNAs, miRNAs, and mRNAs, respectively, were differentially expressed in the DCEF-treated ADSCs compared with untreated ADSCs. Differentially expressed mRNAs were enriched in the MAPK signaling pathway, TNF signaling pathway, and some other pathways. ANXA1, ERRFI1, JAG1, EPHA2, PRR9, and H2AFY2 were related to the keratinocyte differentiation process. Competing endogenous RNA (ceRNA) networks were constructed on the basis of genes in the MAPK signaling pathway. Twenty-one RNAs in the above networks were randomly chosen, and their expression was validated using qRT-PCR, which showed the same expression trends as the RNA sequencing analysis. The MAPK signaling pathway is of great importance in the ADSC processes that occur in a DCEF, including keratinocyte differentiation. Several ceRNAs may participate in the regulation of MAPK signaling. This study may give new insight into the proliferation, migration, and differentiation of ADSCs, which will be valuable for tissue engineering and regenerative medicine.

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Retracted: Effects of microRNA‐494 on proliferation, migration, invasion, and apoptosis of medulloblastoma cells by mediating c‐myc through the p38 MAPK signaling pathway

Cited by 17 publications

References 39 publications

Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway

Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway

Overexpressed microRNA-494 represses RIPK1 to attenuate hippocampal neuron injury in epilepsy rats by inactivating the NF-κB signaling pathway

Changing Expression Profiles and Inclination to Competing Endogenous RNA Networks on MAPK Signaling Pathways of Human Adipose-Derived Stem Cells in a Direct Current Electric Field

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