MicroRNA‑154 functions as a tumor suppressor in non‑small cell lung cancer through directly targeting B‑cell‑specific Moloney murine leukemia virus insertion site 1

Liu, Sida; Yang, Yang; Chen, Lu; Liu, Danwei; Han, Dongyi

doi:10.3892/ol.2018.8595

Cited by 10 publications

(10 citation statements)

References 27 publications

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“…In another study by Xu et al, E2F transcription factor 5 protein (E2F5) was introduced as a direct target of miR-154, with reciprocal relationship between these two parameters in in neoplastic cells of breast [14]. Additionally, reduced levels of miR-154 and its association with aggressive clinicopathological characteristics have been reported in glioma, colorectal, prostate and non-small cell lung cancers [24–27].…”

Section: Discussionmentioning

confidence: 99%

Suppression of nicotinamide phosphoribosyltransferase expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

et al. 2019

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BackgroundNicotinamide phosphoribosyltransferase (NAMPT) enzyme acts as the major enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis salvage pathway. Deregulation of NAD could be associated with progression of several cancers such as breast cancer. Here, the consequence of NAMPT inhibition by miR-154 was investigated on breast cancer cells.MethodsMDA-MB-231 and MCF-7 cancer cell lines were transfected with the mimic and inhibitors of miR-154-5p and their corresponding negative controls. Consequently, levels of NAMPT and NAD were assayed employing qRT-PCR, Western blotting and enzymatic method, respectively. Subsequently, flow cytometry and colorimetric methods were performed to evaluate apoptosis and cell viability. Bioinformatics analyses as well as luciferase assay were done to investigate whether the 3′-UTR of NAMPT is directly targeted by miR-154.ResultsAccording to the obtained results, NAMPT was recognized as a target for binding of miR-154 and the levels of this miRNA was inversely associated with both mRNA and protein levels of NAMPT in breast cancer cell lines. Functionally, miR-154 inhibited the NAD salvage pathway leading to a remarkable decrease in cell viability and increased rate of cell death. When breast cancer cells were simultaneously treated with doxorubicin and miR-154 mimic, cell viability was considerably reduced compared to treatment with doxorubicin alone in both cell lines.ConclusionsIt was concluded that the inhibition of NAD production by miR-154 might be introduced as an appropriate therapeutic approach in order to improve breast cancer outcome either alone or in combination with other conventional chemotherapeutic agents.

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Section: Discussionmentioning

confidence: 99%

Suppression of nicotinamide phosphoribosyltransferase expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

et al. 2019

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“…None of the controls significantly affected the luciferase activity. Additionally, reduced levels of miR-154 and its association with aggressive clinicopathological carachteristics have also been reported in glioma, colorectal, prostate and non-small cell lung cancers (23)(24)(25)(26)).…”

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

confidence: 86%

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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“…For example, miR-154 functions as a tumor suppressor in non-small cell lung cancer by directly targeting BMI-1. 42 Xu et al reported that miR-154 inhibits the growth and invasion of breast cancer cells by targeting E2F5. 43 It was also reported that ZEB2 and RUNX2 act as targets of miR-154 in non-small cell lung cancer.…”

Section: Discussionmentioning

confidence: 99%

P53/miR-154 Pathway Regulates the Epithelial-Mesenchymal Transition in Glioblastoma Multiforme Cells by Targeting TCF12

Zhu¹,

Yang²,

Wang³

et al. 2021

NDT

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Purpose Glioblastoma multiforme (GBM) is an aggressive brain tumor with a rather short survival time. Mutation of p53 has been observed and reported to play critical roles in the progression of GBM. However, the pathological mechanisms are still unclear. This study was designed to identify the role of miR-154 in mediating the biological functions of p53 in glioblastoma multiforme. Methods In the current study, the expression of miR-154 in GBM tissue samples and cell lines with wt-p53 or mutant p53 was evaluated. The functions of miR-154 in tumor migration, invasion and epithelial-mesenchymal transition were analyzed in vitro. A luciferase reporter assay was used to identify the target of miR-154. Results We found that expression of miR-154 was much lower in patient tissues with mutant p53. Further study revealed that p53 was a transcription factor of miR-154 and that the R273H mutation led to its inactivation. In addition, overexpression of miR-154 remarkably suppressed cell migration, invasion and EMT in vitro and tumor growth in vivo. Moreover, TCF12 was proven to be a direct target of miR-154, and the tumor suppressive effect of miR-154 was reversed by TCF12. Conclusion Overall, miR-154, which was regulated by wt-p53, inhibited migration, invasion and EMT of GBM cells by targeting TCF12, indicating that miR-154 may act as a biomarker and that the p53/miR-154/TCF12 pathway could be a potential therapeutic target for GBM.

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MicroRNA‑154 functions as a tumor suppressor in non‑small cell lung cancer through directly targeting B‑cell‑specific Moloney murine leukemia virus insertion site 1

Cited by 10 publications

References 27 publications

Suppression of nicotinamide phosphoribosyltransferase expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Suppression of nicotinamide phosphoribosyltransferase 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

P53/miR-154 Pathway Regulates the Epithelial-Mesenchymal Transition in Glioblastoma Multiforme Cells by Targeting TCF12

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