WNT7A Regulation by miR-15b in Ovarian Cancer

MacLean, James A.; King, Mandy L.; Okuda, Hiroshi; Hayashi, Kanako

doi:10.1371/journal.pone.0156109

Cited by 41 publications

(36 citation statements)

References 27 publications

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“…Aberrant regulation of miR-15b plays a key role in cell proliferation, angiogenesis and metastasis in a variety of tumours [26]. According to the previous studies, miR-15b has displayed decreased expression [6][7][8][9][10][11][12] or increased expression [17][18][19][20][21] in human tumours. Even, miR-15b harbours the opposite expression levels in the same tumour tissues, such as glioma [7,18], indicating that its expression level is related with the specific types of tumour tissues.…”

Section: Discussionmentioning

confidence: 99%

miR‐15b‐5p facilitates the tumorigenicity by targeting RECK and predicts tumour recurrence in prostate cancer

Chen

Lü

Zhang

et al. 2018

J Cellular Molecular Medi

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MicroRNAs (miRNAs) have been reported to participate in many biological behaviours of multiple malignancies. Recent studies have shown that miR‐15b‐5p (miR‐15b) exhibits dual roles by accelerating or blocking tumour progression. However, the molecular mechanisms by which miR‐15b contributes to prostate cancer (PCa) are still elusive. Here, miR‐15b expression was found significantly up‐regulated in PCa in comparison with the normal samples and was positively correlated with age and Gleason score in patients with PCa. Notably, PCa patients with miR‐15b high expression displayed a higher recurrence rate than those with miR‐15b low expression (P = 0.0058). Knockdown of miR‐15b suppressed cell growth and invasiveness in 22RV1 and PC3 cells, while overexpression of miR‐15b reversed these effects. Then, we validated that RECK acted as a direct target of miR‐15b by dual‐luciferase assay and revealed the negative correlation of RECK with miR‐15b expression in PCa tissues. Ectopic expression of RECK reduced cell proliferation and invasive potential and partially abrogated the tumour‐promoting effects caused by miR‐15b overexpression. Additionally, miR‐15b knockdown inhibited tumour growth activity in a mouse PCa xenograft model. Taken together, our findings indicate that miR‐15b promotes the progression of PCa cells by targeting RECK and represents a potential marker for patients with PCa.

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Section: Discussionmentioning

confidence: 99%

miR‐15b‐5p facilitates the tumorigenicity by targeting RECK and predicts tumour recurrence in prostate cancer

Chen

Lü

Zhang

et al. 2018

J Cellular Molecular Medi

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“…We have found high enrichment of microRNAs after 20 days of Lp (a) treatment in HAVICs. Among those identified were miR-130a and miR-15B, which are known to regulate Wnt signalling [40,41] and are identified as biomarker of atherosclerosis obliterans [42]. miR-154 was found to be a biomarker for CAD [43]; and miR216A has roles in osteogenesis and cholesterol efflux via PI3K/AKT pathway [44,45].…”

Section: Discussionmentioning

confidence: 99%

Gene Expression and Proteomic Profiling of Lp (a)-Induced Signalling Pathways in Human Aortic Valve Interstitial Cells

Yu¹,

Kapur²,

Hamid³

et al. 2018

J Pharmacogenomics Pharmacoproteom

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Aortic valve stenosis is one of the most common valve diseases in the world for which there is currently no pharmacological treatment to prevent or halt disease progression. Recent genetic research has demonstrated a causal association between elevated blood levels of lipoprotein (a) (Lp (a)) and aortic valve calcification, however, the mechanisms by which Lp (a) contributes to aortic valve calcification and stenosis, is unknown. In the present study, we aimed at determining Lp (a)-induced changes in human aortic valve interstitial cells using an integrated bioinformatics approach. The Lp (a)-induced cellular pathways were analysed using microarray gene expression and proteomic data from non-stenotic human aortic valve interstitial cells. Lp (a) treatment induced osteogenic differentiation, extracellular remodeling, extracellular vesicles biogenesis, and apoptosis of human aortic valve interstitial cells. In particular, the Wnt/ β-catenin signalling pathway, a known calcification pathway contributing to aortic valve stenosis, was differentially expressed compared to non-treated cells. Lp (a) also induced the expression of 14-3-3 proteins known to regulate various signalling pathway relevant to aortic valve disease. Elucidating the mechanisms and molecular players that Lp (a) induces in the early stages of the disease to initiate aortic valve calcification could provide insight into potential pharmacological targets for the treatment of this debilitating disease.

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“…MicroRNAs (miRNAs) are a class of endogenous and small noncoding RNAs with 21–23 ribonucleotides, which can induce mRNA degradation or act as repressors of translation through directly binding to a target site in the 3′‐untranslated regions of their target genes. Existing studies found that miRNA mediated gene regulation involved in multiple pathological processes including cell proliferation, differentiation, migration, survival, and tumorigenesis . Recent evidence has shown that miRNAs also plays a vital role in chemotherapeutic resistance.…”

Section: Introductionmentioning

confidence: 99%

Up‐regulation of miR‐497 confers resistance to temozolomide in human glioma cells by targeting mTOR/Bcl‐2

Zhu

Zeng

et al. 2017

Cancer Medicine

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The occurrence of an inherent or acquired resistance to temozolomide (TMZ) is a major burden for patients suffering from glioma. Recently, studies have demonstrated that microRNAs play an important role in the regulation of tumor properties in cancers. However, whether miR‐497 contributes to glioma resistance to chemotherapy is not fully understood. In this study, we showed that the expression of miR‐497 was markedly up‐regulated in TMZ‐resistant glioma cells; high miR‐497 expression level was associated with TMZ‐resistant phenotype of glioma cells. The down‐regulation of miR‐497 in glioma cells enhanced the apoptosis‐induction and growth inhibition effects of TMZ both in vitro and in vivo, whereas promotion of miR‐497 increased the chemosensitization of glioma cells to TMZ. The increased level of miR‐497 in TMZ‐resistant glioma cells was concurrent with the up‐regulation of insulin‐like growth factor 1 receptor (IGF1R)/insulin receptor substrate 1 (IRS1) pathway‐related proteins, that is, IGF1R, IRS1, mammalian target of rapamycin (mTOR), and Bcl‐2. In addition, the knockdown of mTOR and Bcl‐2 reduced the tolerance of glioma cells to TMZ. Our results demonstrated that overexpression of miR‐497 is significantly correlated with TMZ resistance in glioma cells by regulating the IGF1R/IRS1 pathway. Therefore, miR‐497 may be used as a new target for treatment of chemotherapy‐resistant glioma.

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WNT7A Regulation by miR-15b in Ovarian Cancer

Cited by 41 publications

References 27 publications

miR‐15b‐5p facilitates the tumorigenicity by targeting RECK and predicts tumour recurrence in prostate cancer

miR‐15b‐5p facilitates the tumorigenicity by targeting RECK and predicts tumour recurrence in prostate cancer

Gene Expression and Proteomic Profiling of Lp (a)-Induced Signalling Pathways in Human Aortic Valve Interstitial Cells

Up‐regulation of miR‐497 confers resistance to temozolomide in human glioma cells by targeting mTOR/Bcl‐2

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