MiR-429 Determines Poor Outcome and Inhibits Pancreatic Ductal Adenocarcinoma Growth by Targeting TBK1

Song, Bin; Zheng, Kailian; Ma, Hongyun; Liu, An-An; Wei, Jing; Shao, Chenghao; Li, Gang; Jin, Gang

doi:10.1159/000373995

Cited by 33 publications

(27 citation statements)

References 38 publications

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“…By contrast, miR-429 may act as a tumor suppressor in certain cancer types. Song et al (22) reported that miR-429 was frequently downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues and cell lines, and lower miR-429 expression in PDAC tissues significantly correlated with shorter survival of PDAC patients. In addition, overexpression of miR-429 inhibited PDAC cell growth via targeting TANK-binding kinase 1 (22).…”

Section: Discussionmentioning

confidence: 99%

“…Song et al (22) reported that miR-429 was frequently downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues and cell lines, and lower miR-429 expression in PDAC tissues significantly correlated with shorter survival of PDAC patients. In addition, overexpression of miR-429 inhibited PDAC cell growth via targeting TANK-binding kinase 1 (22). Ye et al (23) reported that miR-429 inhibited the migration and invasion of breast cancer cells via inhibition of zinc finger E-box binding homeobox 1 and Crk-like expression.…”

Section: Discussionmentioning

confidence: 99%

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miR-429 promotes the proliferation of non-small cell lung cancer cells via targeting DLC-1

Xiao

Zhou

2016

Oncology Letters

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-429 promotes the proliferation of non-small cell lung cancer cells via targeting DLC-1

Xiao

Zhou

2016

Oncology Letters

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“…Despite the improvement gained from medical advance, PDAC remains one of the highest mortality rates, and very low survival improvements have been made, a rate essentially unchanged over the course of the years [3,4]. Additionally, nearly 80% of patients who present with locally advanced or metastatic diseases have an extremely poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

MiR-221 Promotes Capan-2 Pancreatic Ductal Adenocarcinoma Cells Proliferation by Targeting PTEN-Akt

Yang

Xia

et al. 2016

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs, miRs) have emerged as critical regulators of cancer cell proliferation. The effect of miR-221 on cancer cell growth could be significantly changeable in different cell lines. Although miR-221 was reported to promote the cell growth of pancreatic ductal adenocarcinoma (PDAC) cells, its role in Capan-2 cell line is largely unknown. Methods: Capan-2 cells were transfected with miR-221 mimics, inhibitors, or negative controls. Cell Counting Kit-8 was used to determine cell viability. EdU staining and cell cycle analysis were used to measure cell proliferation. Western blotting was used to detect the expression levels of PTEN and phospho-Akt. The PI3K-Akt pathway activator SC-79 and inhibitor LY294002 were used to perform the rescue experiment in determining cell proliferation. Results: Overexpressing miR-221 significantly increased cell vitality and promoted cell proliferation and G1-to-S phase transition of the cell cycle in Capan-2 cells, while inhibition of miR-221 decreased that. The protein level of PTEN in Capan-2 cells was downregulated by overexpressing miR-221, while upregulated by inhibiting miR-221. Consistently, enhanced phosphorylation of Akt^Ser473 was observed in miR-221 overexpressed Capan-2 cells, and the opposite result was found in miR-221 inhibited cells. LY294002 restored the pro-proliferation effect of miR-221 on Capan-2 cells, while SC-79 had no additional effect on cell proliferation in Capan-2 cells transfected with miR-221 mimics. Conclusion: Our study indicates that miR-221 is an oncogenic miRNA which promotes Capan-2 cells proliferation by targeting PTEN-Akt pathway.

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“…Accumulating evidence has implicated miRNAs as essential regulators of atherosclerosis by targeting key factors in the regulatory pathways [3,23,24]. Specifically, miR-429 has been reporter as a tumor suppressor in various cancers [25][26][27][28][29][30][31][32][33]. Moreover, the role of miR-429 in carcinogenesis has been associated with apoptosis augmentation [34,35].…”

Section: Introductionmentioning

confidence: 99%

Atherosclerosis-Associated Endothelial Cell Apoptosis by MiR-429-Mediated Down Regulation of Bcl-2

Zhang¹,

Tian²,

Wang³

et al. 2015

Cell Physiol Biochem

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Background/Aims: Endothelial cell injury and subsequent apoptosis play a key role in the development and pathogenesis of atherosclerosis, which is hallmarked by dysregulated lipid homeostasis, aberrant immunity and inflammation, and plaque-instability-associated coronary occlusion. Nevertheless, our understanding of the mechanisms underlying endothelial cell apoptosis is still limited. MicroRNA-429 (miR-29) is a known cancer suppressor that promotes cancer cell apoptosis. However, it is unknown whether miR-429 may be involved in the development of atherosclerosis through similar mechanisms. We addressed these questions in the current study. Methods: We examined the levels of endothelial cell apoptosis in ApoE (-/-) mice suppled with high-fat diet (HFD), a mouse model for atherosclerosis (simplified as HFD mice). We analyzed the levels of anti-apoptotic protein Bcl-2 and the levels of miR-429 in the purified CD31+ endothelial cells from mouse aorta. Prediction of the binding between miR-429 and 3'-UTR of Bcl-2 mRNA was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. The effects of miR-429 were further analyzed in an in vitro model using oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs). Results: HFD mice developed atherosclerosis in 12 weeks, while the control ApoE (-/-) mice that had received normal diet (simplified as NOR mice) did not. HFD mice had significantly lower percentage of endothelial cells and significantly higher percentage of mesenchymal cells in the aorta than NOR mice. Significantly higher levels of endothelial cell apoptosis were detected in HFD mice, resulting from decreases in Bcl-2 protein, but not mRNA. The decreases in Bcl-2 in endothelial cells were due to increased levels of miR-429, which suppressed the translation of Bcl-2 mRNA via 3'-UTR binding. These in vivo findings were reproduced in vitro on ox-LDL-treated HAECs. Conclusion: Atherosclerosis-associated endothelial cell apoptosis may result from down regulation of Bcl-2, through increased miR-429 that binds and suppresses translation of Bcl-2 mRNA.

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MiR-429 Determines Poor Outcome and Inhibits Pancreatic Ductal Adenocarcinoma Growth by Targeting TBK1

Cited by 33 publications

References 38 publications

miR-429 promotes the proliferation of non-small cell lung cancer cells via targeting DLC-1

miR-429 promotes the proliferation of non-small cell lung cancer cells via targeting DLC-1

MiR-221 Promotes Capan-2 Pancreatic Ductal Adenocarcinoma Cells Proliferation by Targeting PTEN-Akt

Atherosclerosis-Associated Endothelial Cell Apoptosis by MiR-429-Mediated Down Regulation of Bcl-2

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