MiR-205 inhibits cell apoptosis by targeting phosphatase and tensin homolog deleted on chromosome ten in endometrial cancer ishikawa cells

Zhang, Guiyu; Hou, Xinxin; Li, Yue; Zhao, Meng

doi:10.1186/1471-2407-14-440

Cited by 52 publications

(44 citation statements)

References 30 publications

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“…Although the expression of PTEN is regulated at the level of transcription, miRNA-mediated posttranscriptional downregulation of PTEN has been reported [29, 30]. For example, in many cancers, different miRNAs including miR-18a, miR-32, miR-21, miR-214, miR-205 and several others have been shown to directly target PTEN to promote oncogenesis [22, 31-34]. Overexpression of miR-17-miR-92 cluster containing the PTEN-targeting miR-17-5p and miR-19 in the mouse produced a lymphoproliferative disorder along with glomerular hypertrophy and mesangial expansion; the latter two changes also represent two pathologic features of diabetic nephropathy [35].…”

Section: Discussionmentioning

confidence: 99%

High glucose enhances microRNA-26a to activate mTORC1 for mesangial cell hypertrophy and matrix protein expression

Dey

Bera

Das

et al. 2015

Cellular Signalling

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High glucose milieu inhibits PTEN expression to activate Akt kinase and induces glomerular mesangial cell hypertrophy and matrix protein expression in diabetic nephropathy. Specific mechanism by which high glucose inhibits PTEN expression is not clear. We found that high glucose increased the expression of the microRNA-26a (miR-26a) in mesangial cells. Using a sensor plasmid with 3’UTR-driven luciferase, we showed PTEN as a target of miR-26a in response to high glucose. Overexpression of miR-26a reduced the PTEN protein levels resulting in increased Akt kinase activity similar to high glucose treatment. In contrast, anti-miR-26a reversed high glucose-induced suppression of PTEN with concomitant inhibition of Akt kinase activity. Akt-mediated phosphorylation of tuberin and PRAS40 regulates mTORC1, which is necessary for mesangial cell hypertrophy and matrix protein expression. Inhibition of high glucose-induced miR-26a blocked phosphorylation of tuberin and PRAS40, which lead to suppression of phosphorylation of S6 kinase and 4EBP-1, two substrates of mTORC1. Furthermore, we show that expression of miR-26a induced mesangial cell hypertrophy and increased fibronectin and collagen I (α2) expression similar to that observed with the cells incubated with high glucose. Anti-miR-26a inhibited these phenomena in response to high glucose. Together our results provide the first evidence for the involvement of miR-26a in high glucose-induced mesangial cell hypertrophy and matrix protein expression. These data indicate the potential therapeutic utility of anti-miR-26a for the complications of diabetic kidney disease.

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Section: Discussionmentioning

confidence: 99%

High glucose enhances microRNA-26a to activate mTORC1 for mesangial cell hypertrophy and matrix protein expression

Dey

Bera

Das

et al. 2015

Cellular Signalling

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“…PTEN is another classical tumor-suppressor [149]. It is a target of miR-21 [150, 151], miR-130a [152], miR-222 [153] in CC cells; a target of miR-200 [154, 155], miR-205 [47, 156], miR-429 [155] in EC cells and a target of miR-21 [157], miR-106a [158], miR-205 [159], miR-214 [160] and miR-630 [161] in OC. miR-21 induces OC cell proliferation through its targeting of PTEN [157] as well as PDCD4 [162].…”

Section: Biological Significance Of Mirnas In Gynecologic Cancersmentioning

confidence: 99%

MicroRNAs in gynecological cancers: Small molecules with big implications

et al. 2017

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Gynecological cancers (GCs) are often diagnosed at advanced stages, limiting the efficacy of available therapeutic options. Thus, there remains an urgent and unmet need for innovative research for the efficient clinical management of GC patients. Research over past several years has revealed the enormous promise of miRNAs. These small non-coding RNAs can aid in the diagnosis, prognosis and therapy of all major GCs, viz., ovarian cancers, cervical cancers and endometrial cancers. Mechanistic details of the miRNAs-mediated regulation of multiple biological functions are under constant investigation, and a number of miRNAs are now believed to influence growth, proliferation, invasion, metastasis, chemoresistance and the relapse of different GCs. Modulation of tumor microenvironment by miRNAs can possibly explain some of their reported biological effects. miRNA signatures have been proposed as biomarkers for the early detection of GCs, even the various subtypes of individual GCs. miRNA signatures are also being pursued as predictors of response to therapies. This review catalogs the knowledge gained from collective studies, so as to assess the progress made so far. It is time to ponder over the knowledge gained, so that more meaningful pre-clinical and translational studies can be designed to better realize the potential that miRNAs have to offer.

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“…MiRNA-205 is implicated in reducing the invasive and migratory potential in both breast and prostate cancer cells by increasing E cadherin, although they use different targets 89 . However, in endometrial cancer cells, miRNA-205 high expression is associated with tumor progression and worse prognosis by suppressing phosphatase and tensin homolog (PTEN) 10 .…”

Section: Introductionmentioning

confidence: 99%

Clinical Relevance of microRNA Expressions in Breast Cancer Validated Using the Cancer Genome Atlas (TCGA)

et al. 2017

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Background MicroRNAs (miRNAs) play a critical role in the carcinogenesis and progression of breast cancer. MiRNA-205 has tumor suppressive properties, whereas miRNA-18a has both oncogenic and tumor suppressive roles. MiRNA-744’s role in breast cancer is unknown, but is tumor-suppressive in vitro. We hypothesize that high expression of all three miRNAs is associated with a better survival based on their known functions in breast cancer. Methods All data was obtained from the Cancer Genome Atlas (TCGA). Expression of miRNA-18a, miRNA-205, and miRNA-744 were retrieved from the Genomic Data Commons (GDC) data portal for analyses. After miRNA-specific thresholds were derived and used to group the patients into a high or low expression group, survival data was calculated using the Cox proportional hazard model. Further subanalyses separating the patients based on receptor status and AJCC 7th edition TNM staging were similarly compared. Results 1052/1097 samples logged in TCGA had clinical data and miRNA-sequence datasets on the miRNAs of interest. High expression of miRNA-18a (p=0.079), miRNA-205 (p=0.034) and miRNA-744 (p=0.0135) was associated with a better survival. On subanalysis, estrogen receptor (ER), progesterone receptor (PR) positive, and lymph node negative disease had a statistically significant survival advantage with miRNA-18a, miRNA-205 and miRNA-744 high expression. Conclusions By utilizing a big dataset (TCGA) with sufficient statistical power, we found that high expression of miRNA-18a, miRNA-205, and miRNA-744 in the breast tumor samples were all associated with better overall survival in ER/PR positive, lymph node negative disease supporting their role as a tumor suppressor in breast cancer.

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MiR-205 inhibits cell apoptosis by targeting phosphatase and tensin homolog deleted on chromosome ten in endometrial cancer ishikawa cells

Cited by 52 publications

References 30 publications

High glucose enhances microRNA-26a to activate mTORC1 for mesangial cell hypertrophy and matrix protein expression

High glucose enhances microRNA-26a to activate mTORC1 for mesangial cell hypertrophy and matrix protein expression

MicroRNAs in gynecological cancers: Small molecules with big implications

Clinical Relevance of microRNA Expressions in Breast Cancer Validated Using the Cancer Genome Atlas (TCGA)

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