miR-340 suppresses cell migration and invasion by targeting MYO10 in breast cancer

Chen, Cai‐Ping; Sun, Zong‐Lin; Lü, Xiang; Wu, Wanxin; Guo, Wenli; Lu, Jianju; Han, Chao; Huang, Jian‐Qi; Fang, Ying

doi:10.3892/or.2015.4411

Cited by 42 publications

(38 citation statements)

References 32 publications

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“…Interestingly, making use of miRNA expression analysis and RT-PCR, we also found that level of miR-340 was significantly reduced in ovarian cancer cells compared to relevant normal cells [28]. In addition, several reports have demonstrated that miR-340 was also evidently down-regulated in colorectal cancer, breast cancer, glioblastoma and oral squamous cell carcinoma [29][30][31][32]. Therefore, aberrant regulation of miR-340 was altofrequent of in multiple types of cancer cells and tissues, indicating that decreased miR-340 might play a critical role in tumorigenesis.…”

Section: Discussionmentioning

confidence: 70%

MicroRNA-340 Induces Apoptosis and Inhibits Metastasis of Ovarian Cancer Cells by Inactivation of NF-κB1

Sun

Liu³

2016

Cell Physiol Biochem

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Aims: Aberrant expression of microRNA-340 (miR-340) has been frequently reported in some cancers excluding ovarian cancer (OC). The role and its molecular mechanism of miR-340 in OC have not been reported. Methods: Real-time PCR was performed to detect the expression of miR-340 in OC cell lines. MiR-340 mimic and negative control were transfected into OC cells and the effects of miR-340 on the cell proliferation, cell cycle, apoptosis and metastasis were investigated by Brdu-ELISA assay, flow cytometry, qRT-PCR, Transwell and ELISA assays. Furthermore, protein level of NF-κB1 was measured by Western blotting. Meanwhile, luciferase assays were performed to validate NF-κB1 as miR-340 target in OC cells. Results: In this study, we explored the effects of miR-340 overexpression on apoptosis, invasion and EMT in OC cells. The mRNA level of miR-340 in OC cell lines and tissues was evidently reduced. The miR-340 mimic was transiently transfected into OC cells using Lipofectamine™ 2000 reagent. Subsequently, the Brdu-ELISA results showed that introduction of miR-340 inhibited cell proliferation. Our data also demonstrated that miR-340 mimic arrested cell cycle progression and promoted apoptosis of OC cells. In addition, miR-340 overexpression could also inhibit invasion and EMT of OC cells. qRT-PCR were used to determined the expressions of matrix metalloproteinase-2 and -9 (MMP-2 and -9) in OC cells. Next, we found that NF-κB1 expression was evidently reduced by up-regulation of miR-340. Bioinformatics analysis predicted that the NF-κB1 was a potential target gene of miR-340. Luciferase reporter assay further confirmed that miR-340 could directly target the 3' UTR of NF-κB1. Moreover, overexpression of NF-κB1 in OC cells transfected with miR-340 mimic partially reversed the inhibitory of miR-340 mimic. Conclusion: miR-340 induced cell apoptosis and inhibited metastasis in OC cells by down-regulation of NF-κB1.

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Section: Discussionmentioning

confidence: 70%

MicroRNA-340 Induces Apoptosis and Inhibits Metastasis of Ovarian Cancer Cells by Inactivation of NF-κB1

Sun

Liu³

2016

Cell Physiol Biochem

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“…Examination of the expression status, biological function and underlying mechanisms of specific miRNAs in gastric cancer can contribute to the identification of novel biomarkers and therapeutic targets in human gastric cancer. Previous studies have shown that miR-340 plays an important role in human cancers (8)(9)(10)(11)(12)(13)(14). It was found to inhibit the metastatic behavior of breast cancer cells (14) while it decreased the proliferation and promoted the cell apoptosis of prostate cancer cells (13,18).…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNA-340 (miR-340) has been found to play a critical role in human cancers, including breast (8,9), prostate (10,11), and esophageal cancer (12), hepatocellular carcinoma (13) and glioma (14). Functionally, miR-340 was found to inhibit the migration and invasion of breast cancer cells by inhibiting the Wnt pathway (8).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-340 promotes the tumor growth of human gastric cancer by inhibiting cyclin G2

et al. 2016

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Abstract. Aberrant expression and function of microRNAs (miRNAs) play a critical role in the development and progression of various human cancers including gastric cancer. However, the clinical significance and underlying mechanisms of miR-340 remain largely unknown in gastric cancer. In the present study, we demonstrated that the expression of miR-340 was aberrantly elevated in both gastric cancer tissues and cells. Moreover clinical association analyses disclosed that the elevated level of miR-340 was significantly associated with unfavorable clinicopathological characteristics of the gastric cancer patients, such as poor differentiation, large tumor size and advanced tumor-node-metastasis (TNM) stage. Gastric cancer patients with high expression of miR-340 had prominently shorter overall survival and disease-free survival. Functionally, forced expression of miR-340 promoted cell viability, proliferation, colony formation and cell cycle progression in the SGC-7901 cells, while miR-340 silencing reduced cell viability, proliferation, colony formation and cell cycle progression in MGC-803 cells. Furthermore, in vivo experiments indicated that miR-340 knockdown suppressed the tumor growth of MGC-803 cells. Notably, alteration of miR-340 expression affected the luciferase activity of wildtype 3'-UTR of cyclin G2 (CCNG2) and regulated CCNG2 abundance in gastric cancer cells, indicating that CCNG2 is a direct target of miR-340. Moreover, CCNG2 knockdown eradicated the effects of miR-340 silencing on gastric cancer cells. In conclusion, our data suggest that miR-340 may potentially serve as a novel prognostic biomarker and therapeutic target for gastric cancer.

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“…As the actin bundling protein fascin is also overexpressed in prostate cancer [103], we speculated that when MYO10 is knocked down in PC-3 cells, fascin mislocalises and bundles actin filaments in the cell body. Overexpression levels of MYO10 have been linked to a reduction in levels of miR-340 [104] and to an interaction with mutant p53 [99] in breast cancer. However, we did not find a link between mutant p53 and MYO10 in prostate cancer cells [5].…”

Section: Class 5 6 10 and 19 Myosin Isoformsmentioning

confidence: 99%

How myosin organization of the actin cytoskeleton contributes to the cancer phenotype

Peckham

2016

Biochemical Society Transactions

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The human genome contains 39 genes that encode myosin heavy chains, classified on the basis of their sequence similarity into 12 classes. Most cells express at least 12 different genes, from at least 8 different classes, which are typically composed of several class 1 genes, at least one class 2 gene, and classes 5, 6, 9, 10, 18 and 19. While the different myosin isoforms all have specific and non-overlapping roles in the cell, in combination they all contribute to the organisation of the actin cytoskeleton, and the shape and phenotype of the cell. Over (or under) expression of these different myosin isoforms can have strong effects on actin organisation, cell shape, and contribute to the cancer phenotype as discussed in this review.

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miR-340 suppresses cell migration and invasion by targeting MYO10 in breast cancer

Cited by 42 publications

References 32 publications

MicroRNA-340 Induces Apoptosis and Inhibits Metastasis of Ovarian Cancer Cells by Inactivation of NF-κB1

MicroRNA-340 Induces Apoptosis and Inhibits Metastasis of Ovarian Cancer Cells by Inactivation of NF-κB1

MicroRNA-340 promotes the tumor growth of human gastric cancer by inhibiting cyclin G2

How myosin organization of the actin cytoskeleton contributes to the cancer phenotype

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