microRNA-300/NAMPT regulates inflammatory responses through activation of AMPK/mTOR signaling pathway in neonatal sepsis

Li, Yexuzi; Ke, Junzhong; Chen, Peng; Wu, Fugen; Song, Yukang

doi:10.1016/j.biopha.2018.08.064

Cited by 39 publications

(32 citation statements)

References 22 publications

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“…These findings are consistent with our recent study in which, miR-206 was introduced as a potential inhibitor of NAD biosynthesis in HBC cells via direct binding to NAMPT 3´-UTR (21). Consistently, NAMPT 3´-UTR has been reported in a number of studies, as the potential target for a wide variety of miRNAs in other malignancies and diseases including miR-182 in the ossification of ligamentum flavum (38), miR-300 in neonatal sepsis (39), miR-34a in obesity (40), miR-206 in pancreatic cancer (41), miR-26b in colorectal cancer (42), miR-410 in pulmonary arterial hypertension (PAH) (43) and miR-182 in HIV-1 contaminated cells (44).…”

Section: Mir-154 Regulated Nampt By Direct Binding To Its 3′-utrsupporting

confidence: 92%

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Bolandghamtpour¹,

Nourbakhsh²,

Mousavizadeh

et al. 2019

Preprint

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Background Nicotinamide phosphoribosyltransferase (NAMPT) acts as an important enzyme in the salvage pathway of nicotinamide adenine dinucleotide (NAD) biosynthesis. Deregulation of NAD could be associated with progression of many cancers including breast cancer. Here, we evaluated the effect of NAMPT inhibition via miR-154 on survival of breast cancer cells. Methods Breast cancer cell lines including MCF-7 and MDA-MB-231 were transfected with miR-154-5p mimic, inhibitor and their negative controls. Using real-time PCR and western blotting techniques the expression levels of NAMPT and miR-154 were determined and compared with the untreated cells. NAD levels were measured by an enzymatic method. Subsequently, colorimetric methods and flow cytometry were performed to evaluate cell viability and apoptosis. Bioinformatics analyses were performed to investigate whether NAMPT 3′-UTR is a direct target of miR-154 and the findings were confirmed by luciferase reporter assay. Results According to the obtained results, NAMPT 3′-UTR was identified as a direct target of miR-154 and the levels of this miRNA was inversely associated with NAMPT expression both at mRNA and protein levels in breast cancer cell lines. Functionally, miR-154 inhibited the NAD salvage pathway leading to a remarkable decrease in cell survival and induction of apoptosis. Co-treatment of breast cancer cells with doxorubicin and miR-154 mimic significantly reduced cell viability compared to treatment with doxorubicin alone in both cell lines. Conclusions Hence, it was concluded that the inhibition of NAD production by miR-154 might be introduced as a promising therapeutic strategy for the treatment of breast cancer either alone or in combination with other conventional chemotherapeutic agents.

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Section: Mir-154 Regulated Nampt By Direct Binding To Its 3′-utrsupporting

confidence: 92%

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Bolandghamtpour¹,

Nourbakhsh²,

Mousavizadeh

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…These findings are consistent with our recent study in which, miR-206 was introduced as a potential inhibitor of NAD biosynthesis in HBC cells via direct binding to NAMPT 3´-UTR (33). Consistently, NAMPT 3´-UTR has been reported in a number of studies, as the potential target for a wide variety of miRNAs in other malignancies and diseases including miR-182 in the ossification of ligamentum flavum (39), miR-300 in neonatal sepsis (40), miR-34a in obesity (41), miR-206 in pancreatic cancer (42), miR-26b in colorectal cancer (43), miR-410 in pulmonary arterial hypertension (PAH) (44) and miR-182 in HIV-1 contaminated cells (45).…”

Section: Luciferase Reporter Assay Verifying the Predicted Interactiosupporting

confidence: 92%

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Bolandghamtpour

Nourbakhsh²,

Mousavizadeh

et al. 2019

Preprint

View full text Add to dashboard Cite

Background Nicotinamide phosphoribosyltransferase (NAMPT) acts as an important enzyme in the salvage pathway of nicotinamide adenine dinucleotide (NAD) biosynthesis. Deregulation of NAD could be associated with progression of many cancers including breast cancer. Here, we evaluated the effect of NAMPT inhibition via miR-154 on survival of breast cancer cells. Methods Breast cancer cell lines including MCF-7 and MDA-MB-231 were transfected with miR-154 mimic, inhibitor and their negative controls. Using real-time PCR and western blotting techniques the expression levels of NAMPT and miR-154 were determined and compared with the untreated cells. NAD levels were measured by an enzymatic method. Subsequently, colorimetric methods and flow cytometry were performed to evaluate cell viability and apoptosis. Bioinformatics analyses were performed to investigate whether NAMPT 3′-UTR is a direct target of miR-154 and the findings were confirmed by luciferase reporter assay. Results According to the obtained results, NAMPT 3′-UTR was identified as a direct target of miR-154 and the levels of this miRNA was inversely associated with NAMPT expression both at mRNA and protein levels in breast cancer cell lines. Functionally, miR-154 inhibited the NAD salvage pathway leading to a remarkable decrease in cell survival and induction of apoptosis. Co-treatment of breast cancer cells with doxorubicin and miR-154 mimic significantly reduced cell viability compared to treatment with doxorubicin alone in both cell lines. Conclusions Hence, it was concluded that the inhibition of NAD production by miR-154 might be introduced as a promising therapeutic strategy for the treatment of breast cancer either alone or in combination with other conventional chemotherapeutic agents.

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“…Nampt is involved in many important biological processes, including survival, apoptosis, metabolism and angiogenesis (16). As a cytokine, an elevated concentration of Nampt has been observed in several inflammatory and autoimmune disorders, such as sepsis, atherosclerosis, systemic lupus erythematosus and Crohn's disease (17)(18)(19)(20). Previous studies have demonstrated an elevated plasma Nampt concentration in Hashimoto's thyroiditis (HT) patients (14).…”

Section: Discussionmentioning

confidence: 99%

Role of Nampt overexpression in a rat model of Hashimoto's thyroiditis and its mechanism of action

Tang

Wei

et al. 2020

Exp Ther Med

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The present study was designed to investigate the role of nicotinamide phosphoribosyltransferase (Nampt) overexpression in a rat model of Hashimoto's thyroiditis (HT) and its mechanism of action. A rat model of HT was constructed, and the HT rats were injected with an adenoviral expression vector carrying the Nampt gene. The expression of Nampt and Toll-like receptor 4 (TLR4) in thyroid tissues was examined using immunohistochemistry (IHC), RT-qPCR and western blot analyses. Serum anti-thyroglobulin antibodies (TGAb) and anti-thyroid peroxidase antibodies (TPOAb) were measured using chemiluminescence method. Hematoxylin and eosin (H&E) and IHC staining of the rat thyroid tissues showed destroyed thyroid follicles and monocyte infiltration, as well as increased Nampt expression in the thyroid tissues of rats with HT. Furthermore, it was found that Nampt overexpression led to increased severity of inflammatory infiltration in thyroid tissues and increased levels of TPOAb in the serum of HT rats; however, the serum TGAb level was not affected by Nampt overexpression. In addition, Nampt overexpression promoted TLR4 expression in HT rats. In conclusion, it was demonstrated that Nampt was strongly expressed in the capillary region of HT rats thyroid tissues. The Nampt mRNA level was increased but the Nampt protein level was decreased in the thyroid tissues of rats with HT. Nampt overexpression has a promotive effect on HT progression, and this effect was related to TLR4. This study suggests that inhibition of Nampt activity may be valuable in the treatment of HT.

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microRNA-300/NAMPT regulates inflammatory responses through activation of AMPK/mTOR signaling pathway in neonatal sepsis

Abstract: Our study provides evidence indicating that overexpressedmiR-300 enhances autophagy by targeting NAMPT through activation of the AMPK/mTOR signaling pathway in septic mouse models, indicating it may serve as a potential therapeutic target for sepsis.

Cited by 39 publications

References 22 publications

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Role of Nampt overexpression in a rat model of Hashimoto's thyroiditis and its mechanism of action

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