Consort

Wang, Lan; Tian, Han; Yuan, Jie; Wang, Hongmei; Wu, Jueheng; Zhu, Xun

doi:10.1097/md.0000000000002228

Cited by 27 publications

(15 citation statements)

References 44 publications

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“…Increasing evidence shows that this pathway that once exhibited abnormalities can also participate in the potential mechanism of PD [12]. Beta-catenin is a crucial molecule in the Wnt signaling pathway and plays a significant role in cell adhesion, growth, invasion, and metastasis [14]. Glycogen synthase kinase 3β (GSK-3β) has been shown to participate in PD, since it can affect the central nervous system and neuronal apoptosis [15, 16].…”

Section: Introductionmentioning

confidence: 99%

Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

Han

Wen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease, and recent studies suggested that oxidative stress (OS) contributes to the cascade that leads to dopamine cell degeneration in PD. In this study, we hypothesized that salidroside (SDS) offers protection against OS injury in 6-hydroxydopamine (6-OHDA) unilaterally lesioned rats as well as the underlying mechanism. Methods: SDS and LiCl (activators of the Wnt/β-catenin signaling pathway) administration alone and in combination with 6-OHDA injection in rats was performed 3 days before modeling for 17 consecutive days to verify the regulatory mechanism by which SDS affects the Wnt/β-catenin signaling pathway as well as to evaluate the protective effect of SDS on PD in relation to OS in vivo. In addition, pheochromocytoma 12 (PC12) cells were incubated with 10 µmol/L SDS or LiCl alone or with both in combination for 1 h followed by a 24-h incubation with 100 µmol/L 6-OHDA to obtain in vitro data. Results: In vivo the administration of LiCl was found to ameliorate behavioral deficits and dopaminergic neuron loss; increase superoxide dismutase (SOA) activity, glutathione peroxidase (GSH-Px) levels, and glycogen synthase kinase 3β phosphorylation (GSK-3β-Ser9); reduce malondialdehyde (MDA) accumulation in the striatum and the GSK-3β mRNA level; as well as elevate β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-injected rats. This SDS treatment regimen was found to strengthen the beneficial effect of LiCl on 6-OHDA-injected rats. In vitro LiCl treatment decreased the toxicity of 6-OHDA on PC12 cells and prevented apoptosis. Additionally, LiCl treatment increased SOA activity, GSH-Px levels, and GSK-3β-Ser9 phosphorylation; decreased MDA accumulation in the striatum and GSK-3β mRNA levels; as well as increased β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-treated PC12 cells. Additionally, SDS treatment increased the protective effect of LiCl on 6-OHDA-treated PC12 cells. Conclusion: Evidence from experimental models suggested that SDS may confer neuroprotection against the neurotoxicity of 6-OHDA in response to OS injury and showed that these beneficial effects may be related to regulation of the Wnt/β-catenin signaling pathway. Therefore, SDS might be a potential therapeutic agent for treating PD.

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Section: Introductionmentioning

confidence: 99%

Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

Han

Wen

et al. 2018

Cell Physiol Biochem

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“…Furthermore, Zeng et al (61) identified a negative correlation trend between miR-204-5p and SIX homeobox 1 (Six1) expression in BC tissue samples, and when miR-204-5p mimics or Six1 siRNA was transfected, the expression of chromodomain helicase DNA binding protein 1 was markedly increased, thus enhancing epithelial-mesenchymal transition and affecting the invasion and migration of BC cells (61). Various target genes of miR-204-5p have been confirmed in previous studies, including traditional serrated adenoma, MX dynamin like GTPase 1, thioredoxin interacting protein, Src-associated in mitosis 68 kDa protein and forkhead box A1 (57,62–64). However, more target genes need to be determined.…”

Section: Discussionsupporting

confidence: 52%

Expression and potential molecular mechanisms of miR‑204‑5p in breast cancer, based on bioinformatics and a meta‑analysis of 2,306�cases

et al. 2018

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Breast cancer (BC) is the most common cancer among women worldwide. However, there is insufficient research that focuses on the expression and molecular mechanisms of microRNA (miR)-204-5p in BC. In the current study, data were downloaded from the Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO) and the University of California Santa Cruz (UCSC) Xena databases. They were then used to undertake a meta-analysis that leveraged the standard mean difference (SMD) and summarized receiver operating characteristic (sROC) to evaluate the expression of the precursor miR-204 and mature miR-204-5p in BC. Additionally, an intersection of predicted genes, differentially expressed genes (DEGs) from the TCGA database and the GEO database were plotted to acquire desirable putative genes. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and protein-protein interaction (PPI) network analyses were performed to assess the potential pathways and hub genes of miR-204-5p in BC. A decreased trend in precursor miR-204 expression was detected in 1,077 BC tissue samples in comparison to 104 para-carcinoma tissue samples in the TCGA database. Further, the expression of mature miR-204-5p was markedly downregulated in 756 BC tissue samples in comparison to 76 para-carcinoma tissue samples in the UCSC Xena database. The outcome of the SMD from meta-analysis also indicated that the expression of miR-204-5p was markedly reduced in 2,306 BC tissue samples in comparison to 367 para-carcinoma tissue samples. Additionally, the ROC and sROC values indicated that miR-204-5p had a great discriminatory capacity for BC. In GO analysis, ‘cell development’, ‘cell surface activity’, and ‘receptor agonist activity’ were the most enriched terms; in KEGG analysis, ‘endocytosis’ was significantly enriched. Rac GTPase activating protein 1 (RACGAP1) was considered the hub gene in the PPI network. In conclusion, miR-204-5p may serve a suppressor role in the oncogenesis and advancement of BC, and miR-204-5p may have crucial functions in BC by targeting RACGAP1.

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“…The 68-kDa Src-associated protein in mitosis (SAM68) is a GTPase-activating protein (GAP)-related protein involved in intracellular signal transduction that maintains the self-renewal of breast CSCs via affecting the oncogene serine/arginine-rich splicing factor. By targeting SAM68, miR-204 reduces the stem cell phenotype in breast cancer and neutralizes the tumorigenic effect of Sam68 in vivo [47]. It was also reported that miR-204 suppresses self-renewal, stem cell-associated phenotype, and migration of glioma cells via targeting the stemness-governing transcriptional factor SOX4 and the migration-promoting receptor EphB2 [30].…”

Section: Physiological Functions Of Mir-204mentioning

confidence: 99%

The dual regulatory role of miR-204 in cancer

Pan

2016

Tumor Biol.

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MicroRNAs (miRNAs) are a group of endogenous, small (about 22 nucleotides) non-coding RNAs which negatively regulate gene expressions. As one of them, miR-204 originates from the sixth intron of the transient receptor potential melastatin 3 (TRPM3) gene. Therefore, expression of miR-204 is under the control of the TRPM3 promoter and regulated by genetic and epigenetic mechanisms. miR-204 has been found to play the important roles in development of eyes and adipogenesis. Its pathological functions have been observed in a few diseases including pulmonary arterial hypertension, diabetes, and various types of cancers. It is believed that miR-204 acts as a tumor-suppressor via promoting apoptosis, conferring the resistance of cancer cells to chemotherapy, and suppressing the self-renewal of cancer stem cells (CSCs) and the epithelial to mesenchymal transition (EMT). Expression of miR-204 is repressed by its targets XRN1 and TRKB in prostate cancer and endometrial carcinoma, respectively; therefore, they establish an oncogenic feedback loops that play an important role promoting development of cancer. In this review, we summarize our current knowledge regarding miR-204, including its expression, regulation and biological functions, especially focusing our discussion on its role in tumor development and tumor progression.

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Consort

Abstract: Supplemental Digital Content is available in the text

Cited by 27 publications

References 44 publications

Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

Expression and potential molecular mechanisms of miR‑204‑5p in breast cancer, based on bioinformatics and a meta‑analysis of 2,306�cases

The dual regulatory role of miR-204 in cancer

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