SIRT1 is required for oncogenic transformation of neural stem cells and for the survival of “cancer cells with neural stemness” in a p53-dependent manner

Lee, Ji‐Seon; Park, Jeong-Rak; Kwon, Ok‐Seon; Lee, Tae Hee; Nakano, ﻿Ichiro; Miyoshi, Hiroyuki; Chun, Kukjin; Park, Jong Bae; Lee, Hong Jun; Kim, Seung Up; Cha, Hyuk‐Jin

doi:10.1093/neuonc/nou145

Cited by 38 publications

(37 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Knockdown of Sirt1 was proved to enhance the effectiveness of radiotherapy in CD133+ glioma cells in vitro and in vivo [36]. SIRT1 is also required for p53-dependent oncogenic transformation of neural stem cells [37]. In the present study, we found that Sirt1 overexpression reversed the miR-133b-mediated suppression of U87 cell proliferation and invasion, indicating that Sirt1 acts as a downstream effector of miR-133b in glioma cells.…”

Section: Discussionsupporting

confidence: 60%

miR-133b inhibits glioma cell proliferation and invasion by targeting Sirt1

Zhi-xiong

Yang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

MicroRNAs (miRs) are a class of small non-coding RNAs that function as mediators of gene expression. Dysregulations of miRs have been implicated in the development and progression of glioma. In the present study, we investigated the role of miR-133b in mediating the proliferation and invasion of glioma cells, and the potential mechanism. Real-time RT-PCR results showed that miR-133b expression was significantly decreased in glioma tissues compared with normal brain tissues. Luciferase reporter assay further identified silent information regulator 1 (Sirt1) as a novel direct target of miR-133b in glioma U87 cells. Overexpression of miR-133b suppressed Sirt1 expression and reduced the proliferation and invasion of U87 cells, which could be partly rescued by forced expression of Sirt1. In addition, the Sirt1 mRNA level was significantly higher in glioma tissues than in normal brain tissues, and was inversely correlated with miR-133b level in glioma tissues. In summary, our study sheds light on the regulatory mechanism of miR-133b in glioma growth and metastasis via direct mediation of Sirt1 expression, and suggests that Sirt1 may serve as a potential therapeutic target for glioma.

show abstract

Section: Discussionsupporting

confidence: 60%

miR-133b inhibits glioma cell proliferation and invasion by targeting Sirt1

Zhi-xiong

Yang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

show abstract

“…SIRT1 is involved in multiple disease processes that include cancer (106, 111-113), vascular disease (39, 114-117), altered cellular metabolism (12, 102, 103, 118, 119), diabetes (18, 120-123), and neurodegenerative disorders (106, 124, 125). Many of these processes require the modulation of autophagy by SIRT1 (12, 40, 126, 127).…”

Section: Circadian Rhythm Mtor and Sirt1mentioning

confidence: 99%

Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer

Maiese¹

2017

CNR

View full text Add to dashboard Cite

Background The mammalian circadian clock and its associated clock genes are increasingly be recognized as critical components for a number of physiological and disease processes that extend beyond hormone release, thermal regulation, and sleep-wake cycles. New evidence suggests that clinical behavior disruptions that involve prolonged shift work and even space travel may negatively impact circadian rhythm and lead to multi-system disease. Methods In light of the significant role circadian rhythm can hold over the body's normal physiology as well as disease processes, we examined and discussed the impact circadian rhythm and clock genes hold over lifespan, neurodegenerative disorders, and tumorigenesis. Results In experimental models, lifespan is significantly reduced with the introduction of arrhythmic mutants and leads to an increase in oxidative stress exposure. Interestingly, patients with Alzheimer's disease and Parkinson's disease may suffer disease onset or progression as a result of alterations in the DNA methylation of clock genes as well as prolonged pharmacological treatment for these disorders that may lead to impairment of circadian rhythm function. Tumorigenesis also can occur with the loss of a maintained circadian rhythm and lead to an increased risk for nasopharyngeal carcinoma, breast cancer, and metastatic colorectal cancer. Interestingly, the circadian clock system relies upon the regulation of the critical pathways of autophagy, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) as well as proliferative mechanisms that involve the wingless pathway of Wnt/β-catenin pathway to foster cell survival during injury and block tumor cell growth. Conclusions Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis.

show abstract

“…Targeting WISP1, mTOR, and SIRT1 for the treatment of glucose control in DM as well as the complications of this disease opens exciting prospects to eventually limit the devastating and growing impact DM has on the world’s population. Yet, it is imperative that future work addresses the fine biological control WISP1, mTOR, and SIRT1 hold over metabolism to precisely modulate cellular signaling, since these pathways under specific conditions can yield unwanted clinical outcomes that involve induction of fibrotic tissue injury (161), tumorigenesis (302–305), inflammation (242), progression of neurodegenerative disorders (180, 243), cardiac dysfunction (31), loss of neuronal embryonic stem cells that may limit reparative processes in the nervous system (298, 300), and apoptosis in pancreatic islet cells (206). …”

Section: Future Considerationsmentioning

confidence: 99%

Programming Apoptosis and Autophagy with Novel Approaches for Diabetes Mellitus

Maiese¹

2015

CNR

View full text Add to dashboard Cite

According to the World Health Organization, diabetes mellitus (DM) in the year 2030 will be ranked the seventh leading cause of death in the world. DM impacts all systems of the body with oxidant stress controlling cell fate through endoplasmic reticulum stress, mitochondrial dysfunction, alterations in uncoupling proteins, and the induction of apoptosis and autophagy. Multiple treatment approaches are being entertained for DM with Wnt1 inducible signaling pathway protein 1 (WISP1), mechanistic target of rapamycin (mTOR), and silent mating type information regulation 2 homolog) 1 (S. cerevisiae) (SIRT1) generating significant interest as target pathways that can address maintenance of glucose homeostasis as well as prevention of cellular pathology by controlling insulin resistance, stem cell proliferation, and the programmed cell death pathways of apoptosis and autophagy. WISP1, mTOR, and SIRT1 can rely upon similar pathways such as AMP activated protein kinase as well as govern cellular metabolism through cytokines such as EPO and oral hypoglycemics such as metformin. Yet, these pathways require precise biological control to exclude potentially detrimental clinical outcomes. Further elucidation of the ability to translate the roles of WISP1, mTOR, and SIRT1 into effective clinical avenues offers compelling prospects for new therapies against DM that can benefit hundreds of millions of individuals throughout the globe.

show abstract

SIRT1 is required for oncogenic transformation of neural stem cells and for the survival of “cancer cells with neural stemness” in a p53-dependent manner

Cited by 38 publications

References 39 publications

miR-133b inhibits glioma cell proliferation and invasion by targeting Sirt1

miR-133b inhibits glioma cell proliferation and invasion by targeting Sirt1

Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer

Programming Apoptosis and Autophagy with Novel Approaches for Diabetes Mellitus

Contact Info

Product

Resources

About