The PTTG1-targeting miRNAs miR-329, miR-300, miR-381, and miR-655 inhibit pituitary tumor cell tumorigenesis and are involved in a p53/PTTG1 regulation feedback loop

Liang, Haiqian; Wang, Renjie; Diao, Cai-Feng; Li, Jianwei; Su, Jingliang; Zhang, Sai

doi:10.18632/oncotarget.5003

Cited by 75 publications

(76 citation statements)

References 55 publications

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“…Because the parent genes PTTG1 and PTTG2 were previously confirmed to be oncogenes in various cancer types 11, 15, 16, 17 and PTTG3P shares high similarity with these genes (Fig. S1), we suggested that PTTG3P plays a role in modulating PTTG1 or PTTG2 that is similar to previously reported mechanisms 18, 19.…”

Section: Resultssupporting

confidence: 85%

PTTG3P promotes gastric tumour cell proliferation and invasion and is an indicator of poor prognosis

Weng

Wang

et al. 2017

J Cellular Molecular Medi

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Pseudogenes play a crucial role in cancer progression. However, the role of pituitary tumour‐transforming 3, pseudogene (PTTG3P) in gastric cancer (GC) remains unknown. Here, we showed that PTTG3P expression was abnormally up‐regulated in GC tissues compared with that in normal tissues both in our 198 cases of clinical samples and the cohort from The Cancer Genome Atlas (TCGA) database. High PTTG3P expression was correlated with increased tumour size and enhanced tumour invasiveness and served as an independent negative prognostic predictor. Moreover, up‐regulation of PTTG3P in GC cells stimulated cell proliferation, migration and invasion both in vitro in cell experiments and in vivo in nude mouse models, and the pseudogene functioned independently of its parent genes. Overall, these results reveal that PTTG3P is a novel prognostic biomarker with independent oncogenic functions in GC.

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Section: Resultssupporting

confidence: 85%

PTTG3P promotes gastric tumour cell proliferation and invasion and is an indicator of poor prognosis

Weng

Wang

et al. 2017

J Cellular Molecular Medi

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“…It is reported that miR-93 can repress apoptosis after cerebral ischemia via interleukin-1 [38]. Similarly, a previous study proved that miR-381 was overexpressed in the mature brain and normal hippocampal neurons [13], and decreasing miR-381 expression inhibited cell proliferation and invasion [39, 40], from which we inferred that up-regulation of miR-381 inhibited neuronal apoptosis.…”

Section: Discussionsupporting

confidence: 63%

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

Piao¹,

Wu²,

Yang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Acute cerebral ischemia is a manifestation of cerebral vascular insufficiency and has a high mortality. However, the therapy for acute cerebral ischemia is still limited. This study aimed to investigate the effect of microRNA-381 (miR-381) on the repair of nerve injury in rats with acute cerebral ischemia after cerebral lymphatic blockage (CLB) by targeting leucine-rich repeat C4 protein (LRRC4) through the Stromal cell-derived factor-1/CXC chemokine receptor-4 signaling pathway. Methods: Rat models of CLB and middle cerebral artery occlusion (MCAO) were established, and 56 Wistar rats were divided into sham, MCAO, CLB + MCAO, CLB + MCAO + miR-381 inhibitor, CLB + MCAO + miR-381 mimic, CLB + MCAO + AMD3100 and CLB + MCAO + miR-381 mimic + AMD3100 groups. Modified neurological severity score (mNSS was used to determine nerve injury, TTC staining to measure infarction volume, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and flow cytometry to evaluate cell apoptosis, immunofluorescence to measure BrdU-positive cell number, enzyme-linked immunosorbent assay (ELISA) to determine contents of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), nerve growth factor (NGF) and neurite outgrowth inhibitor -A (Nogo-A), Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting to evaluate expression of miR-381, LRRC4, SDF-1, CXCR4, pERK, Slit2 and vascular endothelial growth factor (VEGF). Results: LRRC4 was a target gene of miR-381. Compared with the results in the CLB + MCAO group, mNSS, infarction volume, apoptosis rate and TNF-α, IL-1β, IL-6 and Nogo-A contents as well as LRRC4 expression in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups were increased (those in the CLB + MCAO + AMD3100 group > those in the CLB + MCAO + miR-381 mimic + AMD3100 group), while BrdU-positive cell number, contents of NGF and IL-10, and expression of SDF-1, CXCR4, pERK, Slit2 and VEGF in brain tissues were decreased (those in the CLB + MCAO + AMD3100 group < those in the CLB + MCAO + miR-381 mimic + AMD3100 group). The results in the CLB + MCAO + mimic group were opposite of those in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups. Conclusion: Taken together, we concluded that up-regulation of miR-381 promoted nerve injury repair in acute cerebral ischemia rats after CLB by negatively regulating LRRC4 through activating the SDF-1/CXCR4 signaling pathway.

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“…It is discovered that down-regulation of miR-381 in colon cancer tissues leads to up-regulation of LRH-1 and induces proliferation and invasion of colon cancer cells (22). In addition, miR-381, which is present in the p53/PTTG1 negative feedback loop, can inhibit the growth of pituitary adenomas (23). miR-381 is closely related to MDR1 gene and plays an important role in multidrug resistance (24).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑381 protects myocardial cell function in children and mice with viral myocarditis via targeting cyclooxygenase‑2 expression

Zhang

Sun

et al. 2018

Exp Ther Med

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Abstract. The present study aimed to determine the expression of cyclooxygenase (COX)-2 and microRNA (miRNA/miR)-381 in the blood of children with viral myocarditis (VM), and investigate the association between COX-2 and miR-381 in the occurrence and development of the disease using a mouse model. A total of 26 children with VM (15 boys and 11 girls) were included in the present study. Peripheral blood was collected from all children. The mouse model of VM was constructed by coxsackievirus B3 (CVB3) infection. Peripheral blood and myocardial tissues were collected from all mice for analysis. Reverse transcription-quantitative polymerase chain reaction was used to determine the expression of COX-2 mRNA and miR-381 in serum and myocardial tissues. ELISA was used to measure the content of COX-2 protein in serum from humans and mice, and western blotting was employed to determine the expression of COX-2 protein in myocardial tissues from mice. Contents of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) were evaluated using an automatic biochemical analyzer. A dual luciferase assay was conducted to identify interactions between COX-2 mRNA and miR-381. Children with VM had increased COX-2 levels and decreased miR-381 expression in peripheral blood, compared with those who had recovered from VM. CVB3 infection resulted in damage in the myocardium of mice, and elevated CK-MB and LDH contents. VM model mice exhibited increased COX-2 levels and decreased miR-381 expression in peripheral blood and myocardial tissues compared with normal mice. miR-381 binds to the 3'-untranslated seed regions of both human and mouse COX-2 mRNA to regulate their expression. The present study demonstrated that children with VM have decreased miR-381 expression and elevated COX-2 expression in peripheral blood. miR-381 may inhibit myocardial cell damage caused by CVB3 infection and protect myocardial cell function by targeting COX-2 expression. IntroductionThe incidence of viral myocarditis (VM) is gradually increased in recent years, and attracts the attention of more and more scholars (1). Coxsackievirus B3 (CVB3) is one of the most common viruses that cause VM (2). VM can develop into acute heart failure (3,4). According to available clinical studies, the mortality rate of VM in young people is as high as 21%, and sudden deaths caused by VM or fatal ventricular arrhythmias in children account for about 20% (5,6). However, there have been few effective therapies for VM by now. Current treatment for VM is still focused on the control of cardiac arrhythmia and heart failure. Therefore, it is necessary to study the molecular mechanism of VM.VM is a common infectious disease in pediatric clinical practice. It is caused by viral infection or disturbance of autoimmune system, and characterized by localized or diffuse acute or chronic inflammatory lesions of the myocardium (1,7). In inflammation, cyclooxygenase (COX), especially COX-2 in the COX family, plays an important role. COX-2 is produced after induction by external stimuli (physical...

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The PTTG1-targeting miRNAs miR-329, miR-300, miR-381, and miR-655 inhibit pituitary tumor cell tumorigenesis and are involved in a p53/PTTG1 regulation feedback loop

Cited by 75 publications

References 55 publications

PTTG3P promotes gastric tumour cell proliferation and invasion and is an indicator of poor prognosis

PTTG3P promotes gastric tumour cell proliferation and invasion and is an indicator of poor prognosis

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

MicroRNA‑381 protects myocardial cell function in children and mice with viral myocarditis via targeting cyclooxygenase‑2 expression

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