Tumour‐suppressive <i>microRNA‐224</i> inhibits cancer cell migration and invasion via targeting oncogenic <i>TPD52</i> in prostate cancer

Goto, Yusuke; Nishikawa, Rika; Kojima, Satoko; Chiyomaru, Takeshi; Enokida, Hideki; Inoguchi, Satoru; Kinoshita, Takashi; Fuse, Miki; Sakamoto, Shinichi; Nakagawa, Masayuki; Naya, Yukio; Ichikawa, Tomohiko; Seki, Naohiko

doi:10.1016/j.febslet.2014.04.020

Cited by 75 publications

(45 citation statements)

References 43 publications

(87 reference statements)

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“…Lin et al revealed that reduced expression of miR-224 in prostate cancer was associated with metastasis, high PSA level, high Gleason scores, and poor biochemical recurrence-free survival [25]. Forced expression of miR-224 suppressed prostate cancer cell proliferation, invasion and migration, and promoted cell apoptosis [17,25]. MiR-224 expression has also been found to correlate inversely with tumor stage and lymph node metastasis as well as survival times in colorectal cancer patients [26].…”

Section: Discussionmentioning

confidence: 99%

“…Previous research has identified many oncogenes or tumor suppressor genes as direct targets of miR-224, such as apoptosis inhibitor 5 (API5) [19], Homeobox D10 (HOXD10) [20], SMAD family member 4 (SMAD4) [33], SMAD family member 5 (SMAD5 [18], sarcolemma-associated protein (SLMAP) [18], Type 1 iodothyronine deiodinase (DIO1) [21], tumour protein D52 (TPD52) [17], tribbles homolog 1 (TRIB1) [25], chemokine (C-X-C motif) receptor 4 (CXCR4) [34], hypoxia-inducible factor 1 (HIF1A) [35], Raf kinase inhibitor protein (RKIP) [30], and cell division control protein 42 (CDC42) [36]. It is now clear that miRNAs execute their oncogenic or tumor suppressive functions by regulating the expression of target genes.…”

Section: Discussionmentioning

confidence: 99%

“…Aberrant expression of miR-224 in human malignancies has been demonstrated to play various roles in tumorigenesis. The expression level of miRNA-224 was downregulated in oral cancer [15], ovarian cancer [16], prostate cancer [17], malignant giant cell tumor [18], and glioblastoma [19]; while it was upregulated and functioned as an oncogene in hepatocellular carcinoma [20], clear cell renal cell carcinoma [21], pancreatic cancer [22], and cervical cancer [23]. Notably, a previous study by Yanaihara et al detected decreased miR-224 levels in human lung cancer tissues using miRNA microarray analysis [24].…”

Section: Introductionmentioning

confidence: 99%

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Decreased microRNA-224 and its clinical significance in non-small cell lung cancer patients

et al. 2014

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BackgroundMicroRNA-224 has been proven dysregulated in some human malignancies and correlated with tumor progression. However, its expression and clinical significance in non–small cell lung cancer (NSCLC) is still unclear. Thus, the aim of this study was to explore the effects of miR-224 in NSCLC tumorigenesis and development.MethodsUsing real-time quantitative RT-PCR, we detected miR-224 expression in NSCLC cell lines and primary tumor tissues. The association of miR-224 expression with clinicopathological factors and prognosis was also statistically analyzed. MTT, flow cytometric, Transwell invasion and migration assays, and scratch migration assay were used to test the proliferation, apoptosis, invasion, and migration of NSCLC cells after miR-224 mimics transfection.ResultsMiR-224 expression levels were significantly down-regulated in NSCLC compared to the corresponding noncancerous lung tissues (P <0.001). In addition, decreased miR-224 expression was significantly associated with lymph node metastasis (P = 0.002), advanced TNM stage (P <0.001), and shorter overall survival (P <0.001). Multivariate regression analysis corroborated that down-regulation of miR-224 was an independent unfavourable prognostic factor for patients with NSCLC. Furthermore, transfection of miR-224 mimics in NSCLC A549 cells was able to reduce cell proliferation, invasion, and migration, and promote cell apoptosis.ConclusionsThese findings indicate that miR-224 may act not only as a novel diagnostic and prognostic marker, but also as a potential target for miR-based therapy of NSCLC.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_198

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Decreased microRNA-224 and its clinical significance in non-small cell lung cancer patients

et al. 2014

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“…Several studies showed that TPD52 was overexpressed in several cancers, and function as an oncogenes [29, 30]. Recent study indicated that miR-145-5p and its target gene TPD52 contributed to malignancy progression and in metastasis of brain tumor [31].…”

Section: Discussionmentioning

confidence: 99%

Dual-strand tumor-suppressor microRNA-145 (miR-145-5p and miR-145-3p) coordinately targeted MTDH in lung squamous cell carcinoma

et al. 2016

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Patients with lung adenocarcinoma may benefit from recently developed molecular targeted therapies. However, analogous advanced treatments are not available for patients with lung squamous cell carcinoma (lung SCC). The survival rate of patients with the advanced stage of lung SCC remains poor. Exploration of novel lung SCC oncogenic pathways might lead to new treatment protocols for the disease. Based on this concept, we have identified microRNA-(miRNA) mediated oncogenic pathways in lung SCC. It is well known that miR-145-5p (the guide strand) functions as a tumor suppressor in several types of cancer. However, the impact of miR-145-3p (the passenger strand) on cancer cells is still ambiguous. Expression levels of miR-145-5p and miR-145-3p were markedly reduced in cancer tissues, and ectopic expression of these miRNAs inhibited cancer cell aggressiveness, suggesting that both miR-145-3p as well as miR-145-5p acted as antitumor miRNAs. We identified seven putative target genes (MTDH, EPN3, TPD52, CYP27B1, LMAN1, STAT1 and TXNDC12) that were coordinately regulated by miR-145-5p and miR-145-3p in lung SCC. Among the seven genes, we found that metadherin (MTDH) was a direct target of these miRNAs. Kaplan-Meier survival curves showed that high expression of MTDH predicted reduced survival of lung SCC patients. We investigated pathways downstream from MTDH by using genome-wide gene expression analysis. Our data showed that several anti-apoptosis and pro-proliferation genes were involved in pathways downstream from MTDH in lung SCC. Taken together, both strands of miR-145, miR-145-5p and miR-145-3p are functional and play pivotal roles as antitumor miRNAs in lung SCC.

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“…Previous studies have shown that miR-224 can bind to the tumor suppressors of TNFα-induced protein 1 (TNFAIP1) and Smad4, Raf kinase inhibitor protein (RKIP), apoptosis inhibitor-5 (API-5), PH domain leucine-rich-repeat protein phosphatase 1 (PHLPP1), and PHLPP2 to promote the survival and proliferation of colorectal cancer (CRC) and hepatocellular carcinoma (HCC), but bind to the TRIB1 to promote apoptosis of prostatic cancer cells [7–11]. Furthermore, miR224 binds to the Smad4 and Homeobox D10 (HOXD10) to promote migration of HCC and CRC [8, 12] while it binds to the TPD52 to inhibit migration of prostatic cancer PCa cells [13]. Apparently, the regulatory effects of miR-224 are tissue-specific and depend on the dynamic balance of different signal pathways that regulate proliferation, apoptosis and migration of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-224 inhibits proliferation and migration of breast cancer cells by down-regulating Frizzled 5 expression

Liu

Shen

et al. 2016

Oncotarget

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The Wnt/β-catenin signaling is crucial for the proliferation and migration of breast cancer cells. However, the expression of microRNA-224 (miR-224) in the different types of breast cancers and its role in the Wnt/β-catenin signaling and the proliferation and migration of breast cancer cells are poorly understood. In this study, the levels of miR-224 in different types of breast cancer tissues and cell lines were examined by quantitative RT-PCR and the potential targets of miR-224 in the Wnt/β-catenin signaling were investigated. The effects of altered miR-224 expression on the frequency of CD44+CD24− cancer stem-like cells (CSC), proliferation and migration of MCF-7 and MDA-MB-231 cells were examined by flow cytometry, MTT and transwell migration. We found that the levels of miR-224 expression in different types of breast cancer tissues and cell lines were associated inversely with aggressiveness of breast cancers. Enhanced miR-224 expression significantly reduced the fizzled 5-regulated luciferase activity in 293T cells, fizzled 5 expression in MCF-7 and MDA-MB-231 cells, the β-dependent luciferase activity in MCF-7 cells, and the nuclear translocation of β-catenin in MDA-MB-231 cells. miR-224 inhibition significantly increased the percentages of CSC in MCF-7 cells and enhanced proliferation and migration of MCF-7 cells. Enhanced miR-224 expression inhibited proliferation and migration of MDA-MB-231 cells, and the growth of implanted breast cancers in vivo. Induction of frizzled 5 over-expression mitigated the miR-224-mediated inhibition of breast cancer cell proliferation. Collectively, these data indicated that miR-224 down-regulated the Wnt/β-catenin signaling possibly by binding to frizzled 5 and inhibited proliferation and migration of breast cancer cells.

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Tumour‐suppressive microRNA‐224 inhibits cancer cell migration and invasion via targeting oncogenic TPD52 in prostate cancer

Cited by 75 publications

References 43 publications

Decreased microRNA-224 and its clinical significance in non-small cell lung cancer patients

Decreased microRNA-224 and its clinical significance in non-small cell lung cancer patients

Dual-strand tumor-suppressor microRNA-145 (miR-145-5p and miR-145-3p) coordinately targeted MTDH in lung squamous cell carcinoma

MicroRNA-224 inhibits proliferation and migration of breast cancer cells by down-regulating Frizzled 5 expression

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