Overexpression of miR-199a-5p decreases esophageal cancer cell proliferation through repression of mitogen-activated protein kinase kinase kinase-11 (MAP3K11)

Byrnes, Kimberly A.; Phatak, Pornima; Mansour, Daniel; Xiao, Lan; Zou, Tongtong; Rao, Jaladanki N.; Turner, Douglas J.; Donahue, James M.

doi:10.18632/oncotarget.6752

Cited by 25 publications

(30 citation statements)

References 40 publications

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“…On the other end, in hepatocellular carcinoma [35] and colorectal cancer [36] mir155-5p has demonstrated its ability to resist apoptosis and promotes cellular proliferation, respectively. Intriguingly, although mir199a-5p was found to suppress tumor growth from colorectal cancer cells [37] , papillary thyroid carcinoma [38] , triple-negative breast cancer [39] and proliferation of esophageal cancer cells [40] , its down-regulation was shown to promote prostate adenocarcinoma progression [41] . Furthermore, mir29b-3p has been shown to act as a tumor suppressor in glioblastoma where it can inhibit cell growth and induce apoptosis in vitro [42] .…”

Section: Resultsmentioning

confidence: 99%

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Alwhaibi

Gao

Artham

et al. 2018

Heliyon

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Recent studies indicate a stage-specific, differential role for the oncogene Akt on various cancers. In prostate cancer (PCa), suppression of Akt activity in the advanced stages promoted transforming growth factor-β (TGFβ) pathway-mediated epithelial-to-mesenchymal transition (EMT) and metastasis to the lungs. In the current study, we performed Affymetrix analysis to compare the expression profile of microRNAs in the mouse prostate tissues collected at the prostatic inter-epithelial neoplasia (PIN) stage from Transgenic adenocarcinoma of the mouse (TRAMP)/Akt1+/+ versus TRAMP/Akt1–/– mice, and at the advanced stage from TRAMP/Akt1+/+ mice treated with triciribine (Akt inhibitor) versus DMSO-treated control. Our analysis demonstrates that in the early stage, Akt1 in the TRAMP prostate tumors express a set of miRNAs responsible for regulating cancer cell survival, proliferation, and tumor growth, whereas, in the advanced stages, a different set of miRNAs that promote EMT and cancer metastasis is expressed. Our study has identified novel Akt-regulated signature microRNAs in the early and advanced PCa and demonstrates their differential effects on PCa growth and metastasis.

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Section: Resultsmentioning

confidence: 99%

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Alwhaibi

Gao

Artham

et al. 2018

Heliyon

View full text Add to dashboard Cite

show abstract

“…From the miRNA-mRNA regulatory network constructed in the present study, the regulation of hsa-miR-199a-5p-MAP3K11 was observed. Byrnes et al ( 21 ) demonstrated that miR-199a-5p acts as a tumor suppressor in carcinogenesis, and that its downregulation contributes to enhanced cellular proliferation by targeting MAP3K11. Further details of the results of the present study are presented in Fig.…”

Section: Resultsmentioning

confidence: 99%

Identification of an lncRNA-miRNA-mRNA interaction mechanism in breast cancer based on bioinformatic analysis

Zhang

Wang

et al. 2017

Molecular Medicine Reports

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Non-coding RNAs serve important roles in regulating the expression of certain genes and are involved in the principal biological processes of breast cancer. The majority of studies have focused on defining the regulatory functions of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs/miRs), and few studies have investigated how lncRNAs and miRNAs are transcriptionally regulated. In the present study, based on the breast invasive carcinoma dataset from The Cancer Genome Atlas at cBioPortal, and using a bioinformatics computational approach, an lncRNA-miRNA-mRNA network was constructed. The network consisted of 601 nodes and 706 edges, which represented the complex web of regulatory effects between lncRNAs, miRNAs and target genes. The results of the present study demonstrated that miR-510 was the most potent miRNA controller and regulator of numerous target genes. In addition, it was observed that the lncRNAs PVT1, CCAT1 and linc00861 exhibited possible interactions with clinical biomarkers, including receptor tyrosine-protein kinase erbB-2, estrogen receptor and progesterone receptor, demonstrated using RNA-protein interaction prediction software. The network of lncRNA-miRNA-mRNA interactions will facilitate further experimental studies and may be used to refine biomarker predictions for developing novel therapeutic approaches in breast cancer.

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“…Our functional assays showed that ectopic expression of all members of the miR‐199 family inhibited cancer cell aggressiveness, indicating that the family acted as anti‐tumor miRNA in HNSCC cells. The anti‐tumor function of miR‐199a‐5p was reported in several types of cancers . With regard to miR‐199a‐5p , recent data showed that miR‐199a‐3p was downregulated in osteosarcoma and that restoration of miR‐199a‐3p significantly inhibited CD44 expression .…”

Section: Discussionmentioning

confidence: 99%

Regulation of ITGA3 by the anti‐tumor miR‐199 family inhibits cancer cell migration and invasion in head and neck cancer

et al. 2017

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For patients with head and neck squamous cell carcinoma (HNSCC), survival rates have not improved due to local recurrence and distant metastasis. Current targeted molecular therapies do not substantially benefit HNSCC patients. Therefore, it is necessary to use advanced genomic approaches to elucidate the molecular mechanisms underlying the aggressiveness of HNSCC cells. Analysis of our microRNA (miRNA) expression signature by RNA sequencing showed that the miR‐199 family (miR‐199a‐5p, miR‐199a‐3p, miR‐199b‐5p and miR‐199b‐3p) was significantly reduced in cancer tissues. Ectopic expression of mature miRNA demonstrated that all members of the miR‐199 family inhibited cancer cell migration and invasion by HNSCC cell lines (SAS and HSC3). These findings suggested that both passenger strands and guide strands of miRNA are involved in cancer pathogenesis. In silico database and genome‐wide gene expression analyses revealed that the gene coding for integrin α3 (ITGA3) was regulated by all members of the miR‐199 family in HNSCC cells. Knockdown of ITGA3 significantly inhibited cancer cell migration and invasion by HNSCC cells. Moreover, overexpression of ITGA3 was confirmed in HNSCC specimens, and high expression of ITGA3 predicted poorer survival of the patients (P = 0.0048). Our data revealed that both strands of pre‐miR‐199a (miR‐199a‐5p and miR‐199a‐3p) and pre‐miR‐199b (miR‐199b‐5p and miR‐199b‐3p) acted as anti‐tumor miRNA in HNSCC cells. Importantly, the involvement of passenger strand miRNA in the regulation of cellular processes is a novel concept in RNA research. Novel miRNA‐based approaches for HNSCC can be used to identify potential targets for the development of new therapeutic strategies.

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Overexpression of miR-199a-5p decreases esophageal cancer cell proliferation through repression of mitogen-activated protein kinase kinase kinase-11 (MAP3K11)

Cited by 25 publications

References 40 publications

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Identification of an lncRNA-miRNA-mRNA interaction mechanism in breast cancer based on bioinformatic analysis

Regulation of ITGA3 by the anti‐tumor miR‐199 family inhibits cancer cell migration and invasion in head and neck cancer

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