Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism

Jiang, Xiaohong; Xue, Mei; Fu, Ziyi; Ji, Chenbo; Guo, Xirong; Zhu, Lu; Xu, Li; Pang, Lei; Xu, Meiyu; Qu, Hongming

doi:10.1159/000362957

Cited by 29 publications

(23 citation statements)

References 42 publications

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“…Zhang et al [76] demonstrated that overexpression of miR-378 apparently prevents and treats obesity by activating the muscle pyruvate-phosphoenolpyruvate futile cycle and enhancing lipolysis in adipose tissue. In addition, Jiang et al [80] revealed that miR-378 expression in human adipocytes is induced by adipokines (IL-6, TNFα, leptin, and free fatty acids). Recent experiments provided evidence that obesity induces overexpression of miR-143, which inhibits insulin-stimulated AKT activation leading to impairment of glucose metabolism [81].…”

Section: The Role Of Epigenetics and Developmental Programming In Thementioning

confidence: 99%

Novel Insights in the Metabolic Syndrome in Childhood and Adolescence

Bussler¹,

Penke²,

Flemming³

et al. 2017

Horm Res Paediatr

112

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Metabolic syndrome (MetS) is recognized as an escalating major health risk in adults as well as in children and adolescents. Its prevalence ranges from 6 to 39% depending on the applied definition criteria. To date, there is no consensus on a MetS definition for children and adolescents. However, most authors agree on essential components such as glucose intolerance, central obesity, hypertension, and dyslipidemia; each representing a risk for cardiovascular disease. Recently, associations between MetS and non-alcoholic fatty liver disease, hyperuricemia, and sleep disturbances have emerged. Biomarkers like adipocytokines are a subject of current research as they are implicated in the pathogenesis of the MetS. Epigenetics and gestational programming, especially the role of microRNA, comprise a novel, rapidly developing and promising research focus on the topic of MetS. MicroRNAs are increasingly valued for potential roles in the diagnosis, stratification, and therapeutics of MetS. Early detection of risk factors, screening for metabolic disturbances, and the identification of new therapies are major aims to reduce morbidity and mortality related to MetS. Dietary modification and physical activity are currently the only adopted treatment approaches. Pharmacological therapies and bariatric surgery are still contradictory and, therefore, are only recommended in selected high-risk cases.

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Section: The Role Of Epigenetics and Developmental Programming In Thementioning

confidence: 99%

Novel Insights in the Metabolic Syndrome in Childhood and Adolescence

Bussler¹,

Penke²,

Flemming³

et al. 2017

Horm Res Paediatr

112

View full text Add to dashboard Cite

show abstract

“…It was demonstrated that TNF-α, IL-6, and leptin upregulated miR-378 expression indicating that miR-378 is probably a novel mediator in the development of insulin resistance related to obesity [53]. Also miR-378 was identified to be unregulated through adipokines and cytokines and primarily through sterol-regulatory-element-binding protein (SREBP) and CCAAT/enhancer-binding protein (C/EBP) binding sites in the miR-378 promoter region [54]. Both described inflammatory processes are known to be dysregulated during obesity.…”

Section: Resultsmentioning

confidence: 99%

MicroRNAs Responsible for Inflammation in Obesity

Brettfeld¹,

Maver²,

Aumüller³

et al. 2017

J Endocrinol Metab

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“…HEK293 cells were transfected with 80 ng luciferase reporter vectors and miR-449a mimics (final concentration, 50nM) using the Lipofectamine 3000 (Invitrogen, CA, USA), according to the manufacturer's protocol. After 24 h, luciferase activities were measured using DualLuciferase Reporter System (Berthold), according to the manufacturer's instructions [28].…”

Section: Dual-luciferase Assaymentioning

confidence: 99%

miR-449a Suppresses Tamoxifen Resistance in Human Breast Cancer Cells by Targeting ADAM22

Jen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Most of estrogen receptor positive breast cancer patients respond well initially to endocrine therapies, but often develop resistance during treatment with selective estrogen receptor modulators (SERMs) such as tamoxifen. Altered expression and functions of microRNAs (miRNAs) have been reportedly associated with tamoxifen resistance. Thus, it is necessary to further elucidate the function and mechanism of miRNAs in tamoxifen resistance. Methods: Tamoxifen sensitivity was validated by using Cell Counting Kit-8 in tamoxifen-sensitive breast cancer cells (MCF-7, T47D) and tamoxifen-resistant cells (MCF-7/TAM, T47D/ TAM). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression level of miR-449a in tamoxifen-sensitive/-resistant cells and patient serums. Dual-luciferase assay was used to identify the binding of miR-449a and predicted gene ADAM22. The expression level of ADAM22 was determined by qRT-PCR and western blotting in miR-449a +/- breast cancer cells. Subsequently, rescue experiments were carried out to identify the function of ADAM22 in miR-449a-reduced tamoxifen resistance. Finally, Gene ontology (GO) and Protein-protein interaction analyses were performed to evaluate the potential mechanisms of ADAM22 in regulating tamoxifen resistance. Results: MiR-449a levels were downregulated significantly in tamoxifen-resistant breast cancer cells when compared with their parental cells, as well as in clinical breast cancer serum samples. Overexpression of miR-449a re-sensitized the tamoxifen-resistant breast cancer cells, while inhibition of miR-449a conferred tamoxifen resistance in parental cells. Luciferase assay identified ADAM22 as a direct target gene of miR-449a. Additionally, silencing of ADAM22 could reverse tamoxifen resistance induced by miR-449a inhibition in ER-positive breast cancer cells. GO analysis results showed ADAM22 was mainly enriched in the biological processes of cell adhesion, cell differentiation, gliogenesis and so on. Protein-protein interaction analyses appeared that ADAM22 might regulate tamoxifen resistance through PPARG, LGI1, KRAS and LYN. Conclusion: Decreased miR-449a causes the upregulation of ADAM22, which induces tamoxifen resistance of breast cancer cells. These results suggest that miR-449a, functioning by targeting ADAM22, contributes to the mechanisms underlying breast cancer endocrine resistance, which may provide a potential therapeutic strategy in ER-positive breast cancers.

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Insight into the Effects of Adipose Tissue Inflammation Factors on miR-378 Expression and the Underlying Mechanism

Cited by 29 publications

References 42 publications

Novel Insights in the Metabolic Syndrome in Childhood and Adolescence

Novel Insights in the Metabolic Syndrome in Childhood and Adolescence

MicroRNAs Responsible for Inflammation in Obesity

miR-449a Suppresses Tamoxifen Resistance in Human Breast Cancer Cells by Targeting ADAM22

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