miR-144-3p Induces Cell Cycle Arrest and Apoptosis in Pancreatic Cancer Cells by Targeting Proline-Rich Protein 11 Expression via the Mitogen-Activated Protein Kinase Signaling Pathway

Li, Jian; Sun, Pengxiao; Yue, Zhongyi; Zhang, Dezhong; You, Kun; Wang, Jianguo

doi:10.1089/dna.2017.3656

Cited by 40 publications

(35 citation statements)

References 34 publications

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“…Blue dots indicate congregation of the control group, and red dots indicate congregation of the depression group with mental disorders. 47 miR-144-3p-targeted genes includes Wnt/β-catenin, Nrf2 and MAKP signalling pathways, [48][49][50] which have been verified in the physiology of depression.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, miR‐144‐3p can regulate ataxin 1 (ATXN1) mRNA expression in human cells, and a search of the Genetic Association Database shows that ATXN1 is associated with mental disorders . miR‐144‐3p‐targeted genes includes Wnt/β‐catenin, Nrf2 and MAKP signalling pathways, which have been verified in the physiology of depression.…”

Section: Discussionmentioning

confidence: 99%

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The molecular mechanism underlying GABAergic dysfunction in nucleus accumbens of depression‐like behaviours in mice

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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Depression is the most frequent psychiatric disorder in the world. Recent evidence has shown that stress‐induced GABAergic dysfunction in the nucleus accumbens (NAc) contributed to the pathophysiology of depression. However, the molecular mechanisms underlying these pathological changes remain unclear. In this study, mice were constantly treated with the chronic unpredictable mild stress (CUMS) till showing depression‐like behaviours expression. GABA synthesis, release and uptake in the NAc tissue were assessed by analysing the expression level of genes and proteins of Gad‐1, VGAT and GAT‐3 by qRT‐PCR and Western blotting. The miRNA/mRNA network regulating GABA was constructed based on the bioinformatics prediction software and further validated by dual‐luciferase reporter assay in vitro and qRT‐PCR in vivo, respectively. Our results showed that the expression level of GAT‐3, Gad‐1 and VGAT mRNA and protein significantly decreased in the NAc tissue from CUMS‐induced depression‐like mice than that of control mice. However, miRNA‐144‐3p, miRNA‐879‐5p, miR‐15b‐5p and miRNA‐582‐5p that directly down‐regulated the expression of Gad‐1, VGAT and GAT‐3 were increased. In the mRNA/miRNA regulatory GABA network, Gad‐1 and VGAT were directly regulated by binding seed sequence of miR‐144‐3p, and miR‐15b‐5p, miR‐879‐5p could be served negative post‐regulators by binding to the different sites of VGAT 3′‐UTR. Chronic stress causes the impaired GABA synthesis, release and uptake by up‐regulating miRNAs and down‐regulating mRNAs and proteins, which may reveal the molecular mechanisms for the decreased GABA concentrations in the NAc tissue of CUMS‐induced depression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The molecular mechanism underlying GABAergic dysfunction in nucleus accumbens of depression‐like behaviours in mice

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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“…PRR11 was is a newly identified oncogene, which could promote the proliferation of PC cells. 18 Therefore, we aimed to explore whether downregulation of USP34 could inhibit the proliferation of PANC-1 cells via regulating the expression of PRR11. As shown in Figure 2A, the level of PRR11 was obviously upregulated in PANC-1 cells following infection with lenti-PRR11.…”

Section: Downregulation Of Usp34 Inhibited the Proliferation Of Pc Cementioning

confidence: 99%

<p>Downregulation of USP34 Inhibits the Growth and Migration of Pancreatic Cancer Cells via Inhibiting the PRR11</p>

Lin

Xia

et al. 2020

OTT

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These authors contributed equally to this work Background: Pancreatic cancer (PC) is a highly lethal malignancy worldwide. Our previous study indicated that overexpression of USP34 could promote tumor growth in PC cells. Therefore, this study aimed to further investigate the role of USP34 during the tumorigenesis of PC. Methods: The level of USP34 in PANC-1 and MiaPaCa-2 cells transfected with USP34-shRNAs was detected by RT-qPCR. Moreover, transwell migration and Annexin V/PI analysis were conducted to detect cell migration and apoptosis, respectively. Results: In this study, downregulation of USP34 markedly inhibited proliferation and migration, and induced apoptosis in PANC-1 cells. Moreover, silencing of USP34 obviously downregulated the levels of PRR11 and p-p38 in PANC-1 cells. An in vivo study in nude mice bearing PANC-1 cell xenografts confirmed these results. Conclusion: Downregulation of USP34 could inhibit proliferation and migration in PANC-1 cells via inhibiting PRR11, and inactivating p38 MAPK signaling. Therefore, USP34 might be a potential therapeutic target for the treatment of PC.

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“…Various studies have reported miR‐144‐3p to be an important regulator for apoptosis . A recent study shows that miR‐144‐3p expression is dysregulated in the brain with traumatic brain injury .…”

Section: Introductionmentioning

confidence: 99%

Suppression of microRNA‐144‐3p attenuates oxygen–glucose deprivation/reoxygenation‐induced neuronal injury by promoting Brg1/Nrf2/ARE signaling

Zhao

Cheng

et al. 2018

J Biochem & Molecular Tox

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Accumulating evidence has reported that microRNA-144-3p (miR-144-3p) is highly related to oxidative stress and apoptosis. However, little is known regarding its role in cerebral ischemia/reperfusion-induced neuronal injury. Herein, our results showed that miR-144-3p expression was significantly downregulated in neurons following oxygen-glucose deprivation and reoxygenation (OGD/R) treatment. Overexpression of miR-144-3p markedly reduced cell viability, promoted cell apoptosis, and increased oxidative stress in neurons with OGD/R treatment, whereas downregulation of miR-144-3p protected neurons against OGD/R-induced injury. Brahma-related gene 1 (Brg1) was identified as a potential target gene of miR-144-3p. Moreover, downregulation of miR-144-3p promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased antioxidant response element (ARE) activity. However, knockdown of Brg1 significantly abrogated the neuroprotective effects of miR-144-3p downregulation. Overall, our results suggest that miR-144-3p contributes to OGD/R-induced neuronal injury in vitro through negatively regulating Brg1/Nrf2/ARE signaling.

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miR-144-3p Induces Cell Cycle Arrest and Apoptosis in Pancreatic Cancer Cells by Targeting Proline-Rich Protein 11 Expression via the Mitogen-Activated Protein Kinase Signaling Pathway

Cited by 40 publications

References 34 publications

The molecular mechanism underlying GABAergic dysfunction in nucleus accumbens of depression‐like behaviours in mice

The molecular mechanism underlying GABAergic dysfunction in nucleus accumbens of depression‐like behaviours in mice

<p>Downregulation of USP34 Inhibits the Growth and Migration of Pancreatic Cancer Cells via Inhibiting the PRR11</p>

Suppression of microRNA‐144‐3p attenuates oxygen–glucose deprivation/reoxygenation‐induced neuronal injury by promoting Brg1/Nrf2/ARE signaling

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