miR-429 represses cell proliferation and induces apoptosis in HBV-related HCC

Gao, Huijie; Liu, Chao

doi:10.1016/j.biopha.2014.09.005

Cited by 34 publications

(18 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-429 repressed cell proliferation and induces apoptosis in HBVrelated HCC by targeting NOTCH1 (Gao and Liu, 2014). In our study, we found that the level of miR-429 was elevated at 2 h after PH, and CLIC4, EDEM3 PAWR, PTPN11 and TAP2 were the predicted targets of miR-429.…”

Section: Discussionmentioning

confidence: 74%

Integrative proteomic and microRNA analysis of the priming phase during rat liver regeneration

Geng

Chang

Zang

et al. 2016

Gene

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 74%

Integrative proteomic and microRNA analysis of the priming phase during rat liver regeneration

Geng

Chang

Zang

et al. 2016

Gene

View full text Add to dashboard Cite

“…In another study, miR-429 was found to obviously downregulate much more in hepatitis B virus (HBV)-related hepatocellular carcinoma. MiR-429 was found to directly target NOTCH1 and reduced both mRNA and protein levels of NOTCH1 which stimulated proliferation and suppressed apoptosis in HCC cells [34]. These studies encouraged us to examine a possible role of miRNAs in the development of atherosclerosis through modulation of apoptosis-related proteins.…”

Section: Discussionmentioning

confidence: 95%

“…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]. However, it is unknown whether miR-429 may be involved in the development of atherosclerosis through similar mechanisms.…”

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

View full text Add to dashboard Cite

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.

show abstract

“…Ouyang et al showed that miR-429 promoted cell proliferation through targeting p27Kip1 in human prostate cancer cells [23]. While other studies indicated that miR-429 could suppress cell proliferation via down-regulating BMI1 , E2F3 and NOTCH1 expression [22,24]. The discrepancy of the function of miR-429 in different cell lines may due to the diversity of its targets.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies about miR-200s are mainly focused on the regulation of tumor progression and the epithelial-mesenchymal-transition (EMT) [18,19]. Among them, miR-429 plays an important role in a variety of cellular processes, such as cell invasion, migration, proliferation and apoptosis [20,21,22,23,24,25]. Knockout of miR-200b/a/429 caused high-fat-diet-induced obesity and insulin resistance [26].…”

Section: Introductionmentioning

confidence: 99%

miR-429 Inhibits Differentiation and Promotes Proliferation in Porcine Preadipocytes

Peng

Chen

et al. 2016

IJMS

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are crucial regulatory molecules for adipogenesis. They contribute to the controlling of proliferation and differentiation of preadipocytes. Previous studies revealed an important role of miR-429 in cell invasion, migration, and apoptosis. Our previous work has shown that the expression of miR-429 in subcutaneous fat can be observed in newly born (3-day-old) Rongchang piglets rather than their adult counterparts (180-day-old). This expression pattern suggests that miR-429 might be functionally related to postnatal adipogenesis. However, we currently lack a mechanistic understanding of miR-429 within the context of preadipocyte differentiation. In this study, we investigated the function of miR-429 in porcine subcutaneous and intramuscular preadipocyte proliferation and differentiation. In our porcine preadipocyte differentiation model, miR-429 expression decreased remarkably upon adipogenic induction. Overexpression of miR-429 notably down-regulated the expression of adipogenic marker genes: PPARγ, aP2, FAS and impaired the triglyceride accumulation, while the expression of lipolytic gene ATGL was not affected. In addition, we observed that miR-429 significantly promoted the proliferation of porcine preadipocytes. We also found that miR-429 could directly bind to the 3′-UTRs of KLF9 and p27, which have been well documented to promote preadipocyte differentiation and repress cell cycle progression. Taken together, our data support a novel role of miR-429 in regulating porcine preadipocyte differentiation and proliferation, and KLF9 and p27 are potent targets of miR-429 during these processes.

show abstract

miR-429 represses cell proliferation and induces apoptosis in HBV-related HCC

Cited by 34 publications

References 27 publications

Integrative proteomic and microRNA analysis of the priming phase during rat liver regeneration

Integrative proteomic and microRNA analysis of the priming phase during rat liver regeneration

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

miR-429 Inhibits Differentiation and Promotes Proliferation in Porcine Preadipocytes

Contact Info

Product

Resources

About