Inhibition of MicroRNA-149-5p Induces Apoptosis of Acute Myeloid Leukemia Cell Line THP-1 by Targeting Fas Ligand (FASLG)

Tian, Peijun; Li, Yan

doi:10.12659/msm.899114

Cited by 40 publications

(21 citation statements)

References 32 publications

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“…microRNAs (miRNAs) are a class of short non-coding RNAs, that regulate the expression of target genes by interaction with the 3-un-translated region (3’-UTR) of their mRNAs, resulting in translation inhibition or mRNA degradation [12]. In the cancer studies, miRNAs can function to be oncogenic or tumor-suppressive [13].…”

Section: Introductionmentioning

confidence: 99%

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

Zhang

Feng

2017

Cell Physiol Biochem

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Background/Aims: Pancreatic neuroendocrine tumors (pNETs) are rare neoplasms which arise from pancreatic islet cells. Recently, lncRNA MEG3 has been reported as a tumor suppressor in variety cancers. This study aimed to reveal the functional effects of MEG3 on pNETs which has not been uncovered previously. Methods: The expression of MEG3, miR-183, and BRI3 in BON1 cells were altered by transfection with their specific vectors/shRNA, or mimic/inhibitor. Thereafter, cell viability, apoptosis, the protein expressions of cell cycle related factors, and apoptosis associated factors, as well as cell migration and invasion were respectively assessed by typan blue staining, flow cytometry, western blotting, and transwell assay. Results: MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). MEG3 overexpression decreased BON1 cells viability, invasion, migration, but significantly induced apoptosis. miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. Moreover, BRI3 was a target of miR-183, and BRI3 exhibited a tumor-promoting role possibly via activation of p38/ERK/AKT and Wnt/β-Catenin signaling in BON1 cells. Conclusion: This study demonstrated a tumor suppressive effect of MEG3 in BON1 cells that suppresses tumor cells growth and metastasis. A novel regulatory mechanism has been revealed that modulation of MEG3/miR-183/BRI3 axis may be pivotal in pNET.

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Section: Introductionmentioning

confidence: 99%

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

Zhang

Feng

2017

Cell Physiol Biochem

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“…17 miR-149-5p has been widely reported to exert the suppressor gene in a variety of cancers. 18,19 In addition, miR-1449-5p plays a negative role in the regulation of leucine-rich repeats and immunoglobulin (Ig)-like domains 2 (LRIG2) production. 20 LRIG2 acts as an oncogene, which has been investigated in several types of cancer.…”

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confidence: 99%

LncRNA‐PCAT‐1 promotes non–small cell lung cancer progression by regulating miR‐149‐5p/LRIG2 axis

Li¹,

Wang³

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) are key players in the development and progression of human cancers. The lncRNA PCAT‐1 has been shown to be upregulated in human non–small cell lung cancer (NSCLC); however, its role and molecular mechanisms in NSCLC cell progression remain unclear. Here, we found that the higher expression of PCAT‐1 led to a significantly poorer survival time, and multivariate analysis revealed that PCAT‐1 was an independent risk factor of prognosis in NSCLC. Furthermore, we also found that the knockdown of PCAT‐1 remarkably suppressed cell growth by inducing cell cycle arrest and apoptosis promotion in NSCLC cells. Moreover, the bioinformatics analysis and luciferase reporter assay revealed that PCAT‐1 directly bound to the miR‐149‐5p, which has been reported to act as a tumor suppressor in diverse cancers. In addition, our results confirmed that the tumor‐promoting effects of PCAT‐1 in NSCLC cells are at least partly through negative modulation of miR‐149‐5p. Finally, mechanistic investigations showed that PCAT‐1 upregulated the expression of miR‐149‐5p target gene leucine‐rich repeats and immunoglobulin (Ig)‐like domains 2 (LRIG2) through competitively “spongeing” miR‐149‐5p. Therefore, we concluded that PCAT‐1 may promote the development of NSCLC through the miR‐149‐5p/LRIG2 axis.

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“…MiR-149-5p was upregulated in prostate cancer, acute myeloid leukemia, and glioblastoma. [28][29][30] Other studies demonstrated miR-149-5p functioned as tumor suppressor and was downregulated in gastric cancer, hepatocellular carcinoma and neuroblastoma. [31][32][33] Ke et al showed that miR-149 suppressed lung cancer cell EMT via targeting FOXM1.…”

Section: Discussionmentioning

confidence: 99%

<p>B3GNT3, a Direct Target of miR-149-5p, Promotes Lung Cancer Development and Indicates Poor Prognosis of Lung Cancer</p>

Sun¹,

Liu²,

Lu³

et al. 2020

CMAR

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These authors contributed equally to this work Background: B3GNT3 (β1, 3-N-acetylglucosaminyltransferase-3) belongs to the β3GlcNAcT family and is essential to form extended core 1 oligosaccharides. Previous studies revealed that B3GNT3 expression was dysregulated in multiple cancers. Here, we aimed to understand the expression profile and function of B3GNT3 in lung cancer. Materials and Methods: The expression of B3GNT3 was measured by immunohistochemistry and public database analysis. B3GNT3 was knocked down to evaluate the lung cancer cell proliferation, migration and invasion in in vitro and in vivo tumor formation experiments. miR-149-5p targeting B3GNT3 was identified with TargetScan analysis and confirmed with reporter assay. Overexpression of miR-149-5p was achieved using microRNA mimics and function of microRNA-149-5p/B3GNT3 axis was tested in vitro. Results: B3GNT3 was upregulated in lung cancer, and B3GNT3 overexpression was associated with poor prognosis of lung cancer patients. High expression of B3GNT3 was associated with advanced TNM stages, larger tumor size, tumor metastasis and recurrence. Functionally, we demonstrated that knockdown of B3GNT3 suppressed lung cancer cell growth and invasion in vitro. Knockdown of B3GNT3 suppressed lung cancer development in a xenograft tumor model. Moreover, miR-149-5p was validated to negatively regulate B3GNT3 expression through directly targeting B3GNT3 3ʹ-UTR. Overexpression of miR-149-5p could antagonize the tumorigenesis effect of B3GNT3 in vitro. Conclusion: In summary, our study demonstrated that B3GNT3 overexpression was correlated with poor prognosis of lung cancer patient, indicating that B3GNT3 could be a promising prognostic biomarker for lung cancer. miR-149-5p negatively regulated B3GNT3 expression, which might be utilized for therapeutic target in lung cancer.

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Inhibition of MicroRNA-149-5p Induces Apoptosis of Acute Myeloid Leukemia Cell Line THP-1 by Targeting Fas Ligand (FASLG)

Cited by 40 publications

References 32 publications

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

LncRNA‐PCAT‐1 promotes non–small cell lung cancer progression by regulating miR‐149‐5p/LRIG2 axis

<p>B3GNT3, a Direct Target of miR-149-5p, Promotes Lung Cancer Development and Indicates Poor Prognosis of Lung Cancer</p>

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