Tumor suppressive microRNA-424 inhibits osteosarcoma cell migration and invasion via targeting fatty acid synthase

Long, Xing Hua; Mao, Jian; Peng, Ai; Zhou, Yang; Huang, Shan; Liu, Zhi Li

doi:10.3892/etm.2013.959

Cited by 78 publications

(54 citation statements)

References 36 publications

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“…Few reports have mentioned the effects of miR-424 expression in lung cancer metastasis. However, miR-424 played crucial roles in osteosarcoma cells migration and invasion through targeting fatty acid synthase [30]. Besides, miR-424 is an contributor for prostate cancer metastasis via involving in biological including migration and invasion [31].…”

Section: Discussionmentioning

confidence: 99%

MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1

Zhang

Gao

Yang

et al. 2017

Cell Physiol Biochem

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Background/Aims: This study aimed to investigate the potential roles of miR-424 expression in non-small cell lung cancer (NSCLC) metastasis and growth and its underlying mechanism. Methods: The expression of miR-424 in two NSCLC cell lines (A549 and H1975) was altered by transfection with miR-424 mimic and inhibitor. Effects of miR-424 overexpression and suppression on cells migration, invasion and colony formation were analyzed. Target genes for miR-424 were predicted using bioinformatics method and then verified using luciferase assay. Effects of miR-424 expression on cell migration, invasion and proliferation were reanalyzed on the condition of TNFAIP1 was silenced. Moreover, TNFAIP1 silencing and miR-424 modified A549 cells were subcutaneous injected into node BALB/c mice to confirm the regulation of miR-424 on TNFAIP1 in regulating tumor growth. Results: Compared with the control, miR-424 overexpression significantly increased the migrated and invaded cells, as well as the proliferated colonies. TNFAIP1 was a predicted target gene for miR-424, and was negatively regulated by miR-424. TNFAIP1 silence significantly increased the migrated and invaded cells compared to that in control, while these increases were abolished by miR-424 suppression. Animal experiment further evidenced miR-424 affected tumor growth by regulating TNFAIP1. Conclusions: These data demonstrate that miR-424 may be a contributor for NSCLC progression and metastasis through involving in cell migration, invasion and proliferation via inhibiting TNFAIP1. This study may provide theoretical basis for miR-424 in NSCLC target therapeutic treatment.

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Section: Discussionmentioning

confidence: 99%

MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1

Zhang

Gao

Yang

et al. 2017

Cell Physiol Biochem

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“…Our previous studies (Llobet-Navas et al 2014a,b) and the new data shown here have revealed that this miRNA cluster modulates the expression of at least three well-known oncogenes (CDC25A, BCL-2, and IGF1R) in human and mouse primary breast cancers. Others have also shown that, in other cell types, this cluster targets additional genes involved in cell cycle progression (Nakashima et al 2010;Xu et al 2013b), angiogenesis (Ghosh et al 2010;Nakashima et al 2010), immune response (Xu et al 2016), cell metabolism (Long et al 2013), and cell adhesion (Chong et al 2014). Thus, we propose that aberrant high levels of these targets due to loss of miR-424(322)/ 503 support multiple hallmarks of cancer leading to tumorigenesis (Fig.…”

Section: Discussionmentioning

confidence: 57%

miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy

et al. 2017

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The female mammary gland is a very dynamic organ that undergoes continuous tissue remodeling during adulthood. Although it is well established that the number of menstrual cycles and pregnancy (in this case transiently) increase the risk of breast cancer, the reasons are unclear. Growing clinical and experimental evidence indicates that improper involution plays a role in the development of this malignancy. Recently, we described the miR-424(322)/503 cluster as an important regulator of mammary epithelial involution after pregnancy. Here, through the analysis of ∼3000 primary tumors, we show that miR-424(322)/503 is commonly lost in a subset of aggressive breast cancers and describe the genetic aberrations that inactivate its expression. Furthermore, through the use of a knockout mouse model, we demonstrate for the first time that loss of miR-424(322)/503 promotes breast tumorigenesis in vivo. Remarkably, we found that loss of miR-424(322)/503 promotes chemoresistance due to the up-regulation of two of its targets: BCL-2 and insulin-like growth factor-1 receptor (IGF1R). Importantly, targeted therapies blocking the aberrant activity of these targets restore sensitivity to chemotherapy. Overall, our studies reveal miR-424(322)/ 503 as a tumor suppressor in breast cancer and provide a link between mammary epithelial involution, tumorigenesis, and the phenomenon of chemoresistance.

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“…Study in Wu X et al revealed that the proliferation of human osteosarcoma was suppressed by downregulating Eag1 . Data from Long XH et al indicated that miR-424 suppresses osteosarcoma cell migration and invasion via targeting fatty acid synthase (Long et al, 2013). Another study claimed that the proliferation and invasion of osteosarcoma cells can be inhibited by miR376c by targeting the expression of transforming growth factor-alpha (Jin et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

miRNA-218 Inhibits Osteosarcoma Cell Migration and Invasion by Down-regulating of TIAM1, MMP2 and MMP9

Jin

Cai²,

Liu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

103

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Deregulated miRNAs participate in osteosarcoma genesis. In this study, the expression of miRNA-218 in human osteosarcomas, adjacent normal tissues and Saos-2 human osteosarcoma cells was first assessed. Then the precise role of miRNA-218 in osteosarcoma cells was investigated. Upon transfection with a miR-218 expression vector, the proliferation of Saos-2 human osteosarcoma cells determined using the ATPlite assay was significantly suppressed, whilw migration of Saos-2 cells detected by wound healing and invasion determined using transwells were dramatically inhibited. Potential target genes of miR-218 were predicted and T-cell lymphoma invasion and metastasis 1 (TIAM1) and matrix metalloproteinase 2 (MMP2) and 9 (MMP9) were identified. This was confirmed by western blotting, which showed that miR-218 expression inhibited TIAM1, MMP2 and MMP9 protein expression. Collectively, these data suggest that miR-218 acts as a tumor suppressor in osteosarcomas by down-regulating TIAM1, MMP2 and MMP9 expression.

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Tumor suppressive microRNA-424 inhibits osteosarcoma cell migration and invasion via targeting fatty acid synthase

Cited by 78 publications

References 36 publications

MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1

MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1

miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy

miRNA-218 Inhibits Osteosarcoma Cell Migration and Invasion by Down-regulating of TIAM1, MMP2 and MMP9

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