The Novel miR-7515 Decreases the Proliferation and Migration of Human Lung Cancer Cells by Targeting c-Met

Lee, Ji Min; Yoo, Jung Ki; Yoo, Hai-Soo; Jung, Ho Yong; Lee, Dong Ryul; Jeong, Hoyoung; Oh, Seoung Hun; Chung, Hyung Min; Kim, Jin Kyeoung

doi:10.1158/1541-7786.mcr-12-0355

Cited by 27 publications

(28 citation statements)

References 43 publications

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“…It is well known that in several types of cancer the expression pattern of specific miRNAs is altered [34]. Due to their regulatory role on different signal transduction pathways, miRNAs can have either a tumor suppressor or an oncogenic role during cancer development and progression [35], [57], [58]. Therefore, deregulation of these post-transcriptional regulators results in the altered expression of their direct target genes and consequently erroneous expression of downstream genes.…”

Section: Discussionmentioning

confidence: 99%

MiR-7 Promotes Epithelial Cell Transformation by Targeting the Tumor Suppressor KLF4

et al. 2014

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MicroRNAs (miRNAs) are endogenous small non-coding RNAs that have a pivotal role in the post-transcriptional regulation of gene expression and their misregulation is common in different types of cancer. Although it has been shown that miR-7 plays an oncogenic role in different cellular contexts, the molecular mechanisms by which miR-7 promotes cell transformation are not well understood. Here we show that the transcription factor KLF4 is a direct target of miR-7 and present experimental evidence indicating that the regulation of KLF4 by miR-7 has functional implications in epithelial cell transformation. Stable overexpression of miR-7 into lung and skin epithelial cells enhanced cell proliferation, cell migration and tumor formation. Alteration of these cellular functions by miR-7 resulted from misregulation of KLF4 target genes involved in cell cycle control. miR-7-induced tumors showed decreased p21 and increased Cyclin D levels. Taken together, these findings indicate that miR-7 acts as an oncomiR in epithelial cells in part by directly regulating KLF4 expression. Thus, we conclude that miR-7 acts as an oncomiR in the epithelial cellular context, where through the negative regulation of KLF4-dependent signaling pathways, miR-7 promotes cellular transformation and tumor growth.

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Section: Discussionmentioning

confidence: 99%

MiR-7 Promotes Epithelial Cell Transformation by Targeting the Tumor Suppressor KLF4

et al. 2014

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“…CD151 promote metastasis of cancer cells [26,27]. Also, CD151 is reported to play a role in Met-dependent signalling and the TGF-β signalling [9,28], while c-met play a role in proliferation and migration of human lung and salivary gland cancer cells [29,30]. CD151 is highly expressed in loads of cancer cells and promotes tumour progression [4,31,32].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-124 Suppresses Breast Cancer Cell Growth and Motility by Targeting CD151

Han¹,

Yang²,

Cheng³

et al. 2013

Cell Physiol Biochem

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Background: CD151 is highly expressed in breast cancer cells and has been shown to accelerate breast cancer by enhancing cell growth and motility, but its regulation is poorly understood. To explore post-translation regulation of CD151, for example microRNAs, will be of great importance to claim the mechanism. Methods: A luciferase reporter assay was used to determine whether CD151 was a target of miR-124. The levels of CD151 mRNA were detected by real-time PCR and CD151 protein expression was measured by western blot and flow cytometry. The effects of miR-124 expression on growth, apoptosis, cell cycle and motility of breast cancer cells were determined. Results: We discovered that miR-124 directly targets the 3' untranslated region (3'-UTR) of CD151 mRNAs and suppresses its mRNA expression and protein translation. Both siRNA of CD151 and miR-124 mimics could significantly inhibit proliferation of breast cancer cell lines via cell cycle arrest but does not induce apoptosis. Meanwhile, miR-124 mimics significantly inhibited the motility of breast cancer cells. Conclusion: miR-124 plays a critical role in inhibiting the invasive and metastatic potential of breast cancer cells, probably by directly targeting the CD151 genes. Our findings highlight an important role of miR-124 in the regulation of invasion and metastasis by breast cancer cells and suggest a potential application for miR-124 in breast cancer treatment.

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“…Cellular proliferation rate and viability of labelled cells were tested using the Cell Proliferation Kit II (XTT, Roche Diagnostics, Mannheim, Germany) as previously described [27]. Cell viability was spectrophotometrically quantified after 18 h of incubation with the XTT labelling reagents by measuring absorbance using a multi-label plate reader (PerkinElmer, Rodgau, Germany) and additionally by the trypan blue exclusion test.…”

Section: Cell Viabilitymentioning

confidence: 99%

Fluorescence molecular tomography of DiR-labeled mesenchymal stem cell implants for osteochondral defect repair in rabbit knees

et al. 2016

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The Novel miR-7515 Decreases the Proliferation and Migration of Human Lung Cancer Cells by Targeting c-Met

Cited by 27 publications

References 43 publications

MiR-7 Promotes Epithelial Cell Transformation by Targeting the Tumor Suppressor KLF4

MiR-7 Promotes Epithelial Cell Transformation by Targeting the Tumor Suppressor KLF4

MicroRNA-124 Suppresses Breast Cancer Cell Growth and Motility by Targeting CD151

Fluorescence molecular tomography of DiR-labeled mesenchymal stem cell implants for osteochondral defect repair in rabbit knees

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