Aberrant MicroRNA Expression in Endometrial Carcinoma Using Formalin-Fixed Paraffin-Embedded (FFPE) Tissues

Lee, Taek Sang; Jeon, Hye Won; Kim, Yong Beom; Kim, Young A; Kim, Min Ah; Kang, Soon Beom

doi:10.1371/journal.pone.0081421

Cited by 41 publications

(33 citation statements)

References 33 publications

(29 reference statements)

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“…The involvement of miR-382 and miR-410 in the regulation of MMP16 expression has not been studied in cancer yet, but a single report indicated that low levels of miR-382, along with MMP16 up-regulation, contributed to human intervertebral disc degeneration (54). In accordance with our findings, global miRNA expression profiling by Lee et al, performed on four endometrioid adenocarcinoma samples and four normal endometrial tissues, revealed that miR-377, miR-382 and miR-410 were significantly downregulated in tumor samples (55). Similarly, Torres et al found a down-regulation of miR-410 in EC compared to normal endometrium, and reported that microRNA signatures consisting of miR-410/miR-92 or miR-410/miR-200b/miR-92 accurately differentiated between cancerous and healthy tissues (56).…”

Section: Cancer Genomics and Proteomicssupporting

confidence: 93%

Post-transcriptional Regulation of MMP16 and TIMP2 Expression via miR-382, miR-410 and miR-200b in Endometrial Cancer

Rak

Mehlich

Garbicz

et al. 2017

CGP

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Section: Cancer Genomics and Proteomicssupporting

confidence: 93%

Post-transcriptional Regulation of MMP16 and TIMP2 Expression via miR-382, miR-410 and miR-200b in Endometrial Cancer

Rak

Mehlich

Garbicz

et al. 2017

CGP

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“…RT-qPCR was performed on the tissue samples to determine the expression of six candidate miRs, which have been reported to be differentially expressed in EC tissue (12); the current study observed that of the six miRs only miR-337 was differentially expressed ( Fig. 1; P<0.01).…”

Section: Mir-337 Is Overexpressed In Ec Tissuesmentioning

confidence: 57%

“…Lee et al (12) collected EC tissue samples and adjacent non-cancerous tissue samples, and performed an miR microarray assay to compare the expression profiles of the cancerous and adjacent non-cancerous tissues. Numerous miRs were identified to be differentially expressed in the cancerous tissue samples, with certain genes being upregulated and other genes being downregulated, when compared with the non-cancerous controls (12).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of microRNA-337 promotes the proliferation of endometrial carcinoma cells via targeting PTEN

Cai

Liang

et al. 2016

Molecular Medicine Reports

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Abstract. Endometrial carcinoma (EC) is a common malignancy in females. MicroRNAs (miRs) are a class of non-coding RNA that regulate a wide variety of cellular processes, and are important in the development of multiple types of malignancy. In the present study, cancerous and adjacent non-cancerous normal tissue samples were collected from 24 patients diagnosed with EC. Reverse transcription quantitative polymerase chain reaction was performed on the tissue samples to determine the expression levels of six candidate miRs. These miRs have been previously reported to be differentially expressed in EC; however, the present study observed that only miR-337 was differentially expressed. In addition, the current study identified phosphatase and tensin homolog (PTEN) as a target of miR-337 using computational analysis and a luciferase assay. EC cells transfected with miR-337 mimics and anti-PTEN small interfering RNA demonstrated significantly decreased expression of PTEN, markedly increased proliferation and inhibition of cell apoptosis. The results indicate that miR-337 is oncogenic in EC cells, as it suppresses PTEN expression. This may facilitate the development of miR-based prevention or treatment strategies for EC.

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“…Using deep-sequencing analysis, we found that miR-141-3p expression was decreased by 1.26-fold in early PCa compared to that in BPH (P < 0.05), and confirmed a similar 1.17-fold decrease in early PCa compared to that in BPH (P = 0.2053) by qRT-PCR. In addition, miR-141-3p expression levels vary in different tumors, with overexpression observed in bladder [16], urothelial [17], breast [18] [19], ovarian [20], endometrioid [21], cholangiocytes [22] and colorectal cancers [23] and NSCLC [24], while expression is downregulated in gastric cancer [25], hepatocellular carcinomas [26] [27], renal cell carcinoma [28], lymphatic metastatic pancreatic cancer [29], pituitary tumors [30], craniopharyngioma [31], head and neck cancer [32], osteosarcoma [33], and cutaneous T cell lymphoma [34]. These reports provide compelling evidence for a role of miR-141-3p as an oncogene or tumor suppressor in different tumors and at different stages.…”

Section: Discussionmentioning

confidence: 99%

miR-141-3p Suppresses Expression of Androgen Receptors and Functions as a Tumor Suppressor Gene in Prostate Carcinogenesis

Song¹,

Chen²,

Wang³

et al. 2017

IJCM

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Background: Prostate cancer (PCa) is a leading cause of tumor mortality in Western societies. In China, the PCa mortality rate is increasing yearly. Androgen receptors (ARs) and microRNAs (miRNAs) play central roles in prostate carcinogenesis and progression. Methods: To characterize the underlying molecular mechanisms, we compared the miRNA profiles of early PCa (G ≤ 7), advanced PCa (G > 7) and non-tumor prostate tissues using deep-sequencing. The target genes of differentially expressed miRNAs were predicted by bioinformatics analysis and confirmed by luciferase reporter assays and Western blot (WB) and quantitative reverse transcription-PCR (qRT-PCR)analyses. Finally, we performed in vitro functional studies by inducing or inhibiting miR-141-3p expression using an artificial mimic or inhibitor. Results: A computational search implicated the open reading frame (ORF) of AR mRNA as a potential miR-141-3p target site. The qRT-PCR, WB and luciferase reporter assays revealed a reverse regulatory effect of miR-141-3p on AR. Mutation of the potential miR-141-3p binding site in the AR ORF resulted in a loss of responsiveness to the corresponding miRNA. Moreover, miR-141-3p expression levels were unchanged in early PCas, but were obviously increased in advanced PCas. MiR-141-3p overexpression inhibited RWPE-1 cell proliferation, mobility, and prohibited the entry of cells into the G2-S-M phase; miR-141-3p inhibition had the inverse effects. At the same time, we tested miR-141-3p's functions in PC-3 and VCaP prostate cancer cell lines. Conclusions: Taken together, our results indicate that miR-141-3p targets AR and its downstream signaling pathways, and functions as a tumor suppressor miR in PCa carcinogenesis by suppressing cell growth and mobility, but the effect is not significant in maglinant PCas. MiR-141-3p is implicated as a novel therapeutic target for early PCa.

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Aberrant MicroRNA Expression in Endometrial Carcinoma Using Formalin-Fixed Paraffin-Embedded (FFPE) Tissues

Cited by 41 publications

References 33 publications

Post-transcriptional Regulation of MMP16 and TIMP2 Expression via miR-382, miR-410 and miR-200b in Endometrial Cancer

Post-transcriptional Regulation of MMP16 and TIMP2 Expression via miR-382, miR-410 and miR-200b in Endometrial Cancer

Upregulation of microRNA-337 promotes the proliferation of endometrial carcinoma cells via targeting PTEN

miR-141-3p Suppresses Expression of Androgen Receptors and Functions as a Tumor Suppressor Gene in Prostate Carcinogenesis

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