MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma

Fu, Yi; Cao, Fuhua

doi:10.2147/ott.s92314

Cited by 36 publications

(40 citation statements)

References 16 publications

(16 reference statements)

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“…The increased methylation of miR-125a promoter may lead to a decrease in transcription factor recruitment to the promoter, thus resulting in a decrease in the expression of miR-125a. Previous studies have shown that miR-125a plays a role as a tumor suppressor genes in prostate cancer [15], glioblastoma [16, 17], breast cancer [18], liver cancer [7, 19], gastric cancer [11, 20] and cervical cancer [21, 22]. Wang et al found that EGFR inhibited the invasion of lung cancer cells by activating miR-125a, and miR-125a could also inhibit the proliferation of vascular endothelial cells [23].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

Tao

Shen

Luo

et al. 2017

Cell Physiol Biochem

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Background/Aims: Increasing evidence has shown that miR-125a plays important role in human cancer progression. However, little is known about the function of miR-125a in osteosarcoma. Methods: The expression of miR-125a in osteosarcoma tissues and cell lines were examined by qRT-PCR. The biological role of miR-125a in osteosarcoma cell proliferation was examined in vitro. The targets of miR-125a were identified by a dual-luciferase reporter assay. Results: The results showed that the expression of miR-125a expression is significantly lower in osteosarcoma tissues and cell lines. Survival curves showed that the survival of patients in high miR-125a expression was significantly longer than that of patients with low miR-125a expression, and multivariate analysis suggested that miR-125a is an independent prognostic factor for osteosarcoma patients. In addition, it was found in this study that miR-125a can inhibit the growth of osteosarcoma cells. The dual-luciferase reporter assay demonstrated that E2F2 is a novel target gene for miR-125a. In addition, in a recovery experiment, it was shown that miR-125a inhibits the biological function of osteosarcoma cells by inhibiting the expression of E2F2. Conclusion: Our results suggest that miR-125a acts as a tumor suppressor via regulation of E2F2 expression in osteosarcoma progression, and miR-125a may represent a novel therapeutic target for the treatment of osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

Tao

Shen

Luo

et al. 2017

Cell Physiol Biochem

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“…The human gene encoding nuclear apoptosis‐inducing factor 1 (NAIF1) is located on chromosome 9q34.11, and reported to repress the progression of several human cancers . NAIF1 was downregulated or lost in gastric cancer tissues, plays an inhibitory role in the initial steps of gastric cancer genesis .…”

Section: Introductionmentioning

confidence: 99%

“…NAIF1 was downregulated or lost in gastric cancer tissues, plays an inhibitory role in the initial steps of gastric cancer genesis . Fu et al showed that overexpression of NAIF1 had an antitumor effect on prostate cancer cell proliferation and migration . NAIF1 expression level in NSCLC tissues was suppressed, and restoration of NAIF1 in lung cancer cell inhibited cell proliferation and anchorage‐independent survival ability .…”

Section: Introductionmentioning

confidence: 99%

NAIF1 suppresses osteosarcoma progression and is regulated by miR‐128

Kong

Zhang

2018

Cell Biochemistry & Function

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Nuclear apoptosis‐inducing factor 1 (NAIF1) acts as an oncogene and involves in tumorigenesis in several cancers. However, the expression and mechanism of NAIF1 in osteosarcoma remains unclear. In this study, we demonstrated the downregulation of NAIF1 expression in both osteosarcoma tissues and cell lines. We next explored the potential role of NAIF1 in osteosarcoma cell proliferation and migration. The result showed that overexpression of NAIF1 evidently suppressed the cell proliferation and invasion of osteosarcoma. Furthermore, we investigated the potential mechanisms accounting for dysregulation of NAIF1 in osteosarcoma. The bioinformatic prediction and luciferase reporter assay revealed that miR‐128 is a direct upstream regulator of NAIF1 and regulates NAIF1 expression by binding the 3′‐UTR of NAIF1. Consistent with previous study, we found that miR‐128 was upregulated in both osteosarcoma tissues and cell lines. Moreover, miR‐128 expression levels were inversely correlated with that of NAIF1 in osteosarcoma tissues. Finally, functional assay showed that miR‐128 significantly suppressed osteosarcoma progression partially mediated by inhibiting NAIF1 expression. These data indicate that the miR‐128 and its target gene NAIF1 played important roles by regulating OS cell proliferation and migration phenotype. Significance of the study Osteosarcoma (OS) is the most common malignant bone tumour and the second leading cause of cancer‐related death affecting children and adolescents. Nuclear apoptosis‐inducing factor 1 (NAIF1) plays an inhibitory role in the initial steps of different carcinomas. However, the expression and mechanism of NAIF1 in osteosarcoma remains unclear. The data of this study indicated that the miR‐128 and its target gene NAIF1 played important roles by regulating OS cell proliferation and migration phenotype. It was demonstrated that NAIF1 would demonstrate important regulative effects and may be a promising therapeutic target of OS.

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“…Up-regulated miR-125a was also reported in prostate cancer [71]. However, other studies have reported under-expression of miR-125a and suggested a tumor suppressive role for this miRNA [72][73][74][75].…”

Section: Figurementioning

confidence: 87%

Integrative Analysis of Transcriptome and MicroRNome Profiles in Cholangiocarcinoma

Severino¹,

Hasimoto²,

Rodrigues³

et al. 2017

J Cancer Sci Ther

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Aim: To identify deregulated expression of miRNAs and target genes in cholangiocarcinoma (CCA), as well as drug-gene interactions that may be useful for patient treatment. Methods:We analyzed quantitative transcriptome and miRNA deep sequencing expression data from 45 samples, 36 CCA and 9 histologically normal biliary tissues, obtained from the public repository The Cancer Genome Atlas (TCGA). Bioinformatic methods were used to identify and integrate differential expression of miRNA and transcriptome profiles in CCA vs. normal tissues. Deregulated miRNA and corresponding target genes were identified and mapped into miRNA-mRNA networks. Results:Results showed 64 differentially expressed miRNAs (48 over and 16 under-expressed) between CCA and corresponding normal biliary tissues. Additionally, 432 genes (180 over and 252 under-expressed) were identified between CCA and normal samples. We identified individual miRNAs with the largest number of gene targets. Among these, miR-125a was over-expressed and had the highest number of direct interactions with 33 mRNA targets. miRNAs miR-122 and miR-139 were the under-expressed miRNAs with the highest number of interactions (9 targets each). miR-122 was found to modulate the expression of the transcription factor FOXM1, known to be involved in tumorigenesis and the matrix metalloproteinase MMP7, an important mediator of tumor invasion. miR-148 and miR-194 were predicted to modulate NQO1, which is up-regulated in cancer and associated with treatment resistance in cholangiocarcinoma. Conclusion:The novelty of our study is the identification of complex deregulated networks of miRNAs and target genes in CCA. miRNAs with a large number of targets may have a higher functional impact on cell regulation. These findings contribute for a better understanding of CCA biology. Identified miRNAs and target genes are potential candidates for the design of validation strategies towards the characterization of clinically applicable biomarkers; such biomarkers may be useful for the development of molecularly-targeted therapeutics that can benefit patients.

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MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma

Cited by 36 publications

References 16 publications

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

NAIF1 suppresses osteosarcoma progression and is regulated by miR‐128

Integrative Analysis of Transcriptome and MicroRNome Profiles in Cholangiocarcinoma

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