miR-16-1-3p targets TWIST1 to inhibit cell proliferation and invasion in NSCLC

Feng, Qing; Dong, Zhen; Zhou, Yong Jin; Zhang, H; Long, Chunxi

doi:10.4149/bll_2018_012

Cited by 18 publications

(18 citation statements)

References 26 publications

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“…miRNAs can be upregulated or downregulated in tumor tissues compared with normal tissues, and they can be divided into tumor promoter and tumor suppressor miRNAs (10). miRNA (miR)-15/16, miR-34 and the miR-200 family are reported to have inhibitory effects on lung cancer; the overexpression of miR-15/16 inhibited non-small cell lung cancer cell proliferation and invasion by regulating TWIST1 (10,11); miR-17-92, miR-222/221 and miR-155 were found to promote the progression of breast cancer, and miR-17-5p promoted breast cancer cell invasion and migration through the inhibition of HMG box-containing protein 1 (10,12).…”

Section: Introductionmentioning

confidence: 99%

miR-92a-3p promotes the proliferation, migration and invasion of esophageal squamous cell cancer by regulating PTEN

Guo

Min

et al. 2019

Int J Mol Med

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Esophageal squamous cell cancer (ESCC) has a high mortality rate. MicroRNA (miR)-92a-3p is considered to be a tumor promotor and an oncomiR. The aim of the present study was to investigate the effect of miR-92a-3p and its target gene on ESCC in terms of proliferation, migration and invasion. Higher expression of miR-92a-3p was detected in the tissues of patients with ESCC, compared with that in normal tissues. In addition, ESCC cell lines had a higher expression of miR-92a-3p compared with normal esophageal cells. A miR-92a-3p mimic was found to promote ESCC cell proliferation and a miR-92a-3p inhibitor was found to reduce ESCC cell proliferation. miR-92a-3p mimic transfection accelerated ESCC cell migration and invasion and decreased ESCC cell apoptosis via the Bax/Bcl-2 pathway and cleaved caspase-3. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was detected as a target of miR-92a-3p by a dual luciferase reporter assay. The overexpression of PTEN not only inhibited ESCC proliferation, migration and invasion, but also promoted ESCC cell apoptosis. PTEN and the miR-92a-3p mimic inhibited and promoted ESCC proliferation, respectively, which may be associated with the PI3K/Akt pathway. The results of the study revealed that miR-92a-3p promoted the proliferation, migration and invasion of ESCC, and the effect of miR-92a-3p on ESCC was realized by regulating PTEN.

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Section: Introductionmentioning

confidence: 99%

miR-92a-3p promotes the proliferation, migration and invasion of esophageal squamous cell cancer by regulating PTEN

Guo

Min

et al. 2019

Int J Mol Med

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“…MiRNA-16-1-3p has been reported to act as a tumor suppressor in osteosarcoma (Maximov et al, 2019), non-small cell lung cancer (NSCLC;Feng et al, 2018) and gastric cancer (Wang et al, 2017). However, the function of miRNA-16-1-3p in breast cancer remains unclear.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Liang²,

Zhang³

et al. 2020

Front. Cell Dev. Biol.

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The Warburg effect (aerobic glycolysis) is a hallmark of cancer and is becoming a promising target for diagnosis and therapy. Phosphoglycerate kinase 1 (PGK1) is the first adenosine triphosphate (ATP)-generating glycolytic enzyme in the aerobic glycolysis pathway and plays an important role in cancer development and progression. However, how microRNAs (miRNAs) regulate PGK1-mediated aerobic glycolysis remains unknown. Here, we show that miR-16-1-3p inhibits PGK1 expression by directly targeting its 3′-untranslated region. Through inhibition of PGK1, miR-16-1-3p suppressed aerobic glycolysis by decreasing glucose uptake, lactate and ATP production, and extracellular acidification rate, and increasing oxygen consumption rate in breast cancer cells. Aerobic glycolysis regulated by the miR-16-1-3p/PGK1 axis is critical for modulating breast cancer cell proliferation, migration, invasion and metastasis in vitro and in vivo. In breast cancer patients, miR-16-1-3p expression is negatively correlated with PGK1 expression and breast cancer lung metastasis. Our findings provide clues regarding the role of miR-16-1-3p as a tumor suppressor in breast cancer through PGK1 suppression. Targeting PGK1 through miR-16-1-3p could be a promising strategy for breast cancer therapy.

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“…miR-16 has been reported to suppress the proliferation, invasion, and metastasis of HCC cells by mediating EMT process [25]. Twist1, identified as the direct target of miR-16, is reportedly to be an important transcription factor for regulating EMT process.…”

Section: Discussionmentioning

confidence: 99%

“…Up-regulation of Twist1 has led to an EMT morphological transition as well as enhanced cell metastasis by mediating the expression E-cadherin, N-cadherin, and metalloproteinase [27, 28, 29]. miR-16 has been demonstrated to inhibit cell invasion and metastasis via inversely regulating Twist1 in some cancers such as gastric cancer and non-small cell lung carcinoma (NSCLC) [25, 26].…”

Section: Discussionmentioning

confidence: 99%

“…Twist1, an important EMT transcription factor known to suppress E-cadherin transcription, is identified as the direct target of miR-16. Twist1 has been suggested to have oncogenic properties and the expressions of miR-16 and Twist1 in cancer cells and tissues were inversely correlated [25, 26]. Evidence shows that Twist1 regulates the expression of several EMT-related genes to mediate tumor cells [27, 28, 29].…”

Section: Introductionmentioning

confidence: 99%

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microRNA-16 via Twist1 inhibits EMT induced by PM2.5 exposure in human hepatocellular carcinoma

Zhang

Zhi-hu

2019

Open Medicine

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AbstractEpidemiological study has confirmed that PM2.5 (particulate matter with an aerodynamic diameter less than 2.5 μm) is associated with the incidence and progression of human hepatocellular carcinoma (HCC). Accordingly, this study was undertaken to investigate the pro-metastatic effects of PM2.5 on human HCC cell line SMMC-7721 in vitro and to explore the underlying mechanisms. CCK-8 assay was performed to examine the effect of PM2.5 on the proliferation of SMMC-7721 cells; scratch wound assay and transwell matrigel system has been used to examine the effect of PM2.5 on the migration and invasion ability of SMMC-7721 cells; furthermore, effect of PM2.5 on epithelial mesenchymal transition (EMT) of SMMC-7721 cells were examined by examining the EMT markers vimentin, ɑ-smooth muscle actin (ɑ-SMA), and E-cadherin; furthermore, the roles of microRNA-16 (miR-16) and its target Twist1 in PM2.5 induced carcinogenic effects were also examined. Results of CCK-8 assay suggested that PM2.5 promoted the proliferation of SMMC-7721 cells in a dose and time dependent manner. PM2.5 also markedly promoted the migration and invasion ability of SMMC-7721 cells. Moreover, epithelial mesenchymal transition (EMT) was also triggered by PM2.5. On the other hand, microRNA-16 (miR-16) and its target Twist1 was found to be mediated by PM2.5, and miR-16 mimic could suppress the metastatic ability of SMMC-7721 cells exposure to PM2.5 via inversely regulating the expression of Twist1. Furthermore, dual Luciferase reporter assay confirmed the specifically binding of miR-16 to the predicted 3′-UTR of Twist1. The present study confirmed the pro-proliferative and pro-metastatic effect of PM2.5 on HCC cell line SMMC-7721. The possible mechanisms were EMT process induced by PM2.5 in SMMC-7721 cells, which was accompanied by a decrease in miR-16 and increase in Twist1 expression.

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miR-16-1-3p targets TWIST1 to inhibit cell proliferation and invasion in NSCLC

Cited by 18 publications

References 26 publications

miR-92a-3p promotes the proliferation, migration and invasion of esophageal squamous cell cancer by regulating PTEN

miR-92a-3p promotes the proliferation, migration and invasion of esophageal squamous cell cancer by regulating PTEN

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

microRNA-16 via Twist1 inhibits EMT induced by PM2.5 exposure in human hepatocellular carcinoma

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