MicroRNA-132 targets PEA-15 and suppresses the progression of astrocytoma in vitro

Geng, Fei; Wu, Jianlin; Lu, Gui-Feng; Liang, Zhi-Ping; Duan, Zhuoli; Gu, Xi

doi:10.1007/s11060-016-2173-2

Cited by 8 publications

(7 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, studies on its effect in glioma were not too much. Some studies proved that miR-132 was an anti-oncogene that inhibited migration and invasion of glioma [ 39 , 40 ]. Nevertheless, its target relationship with NEAT1 has never been revealed except for this study.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of long non-coding RNA NEAT1 inhibits glioma cell migration and invasion via modulation of SOX2 targeted by miR-132

et al. 2018

View full text Add to dashboard Cite

BackgroundA better understanding of the molecular mechanism involving lncRNA-miRNA-mRNA network underlying glioma genesis is beneficial to the treatment of glioma. This study was designed to investigate the role of lncRNA NEAT1, miR-132 and SOX2 interaction in glioma.MethodsMicroarray analysis was conducted to identify the differentially expressed lncRNAs in glioma tissues. The expression levels of NEAT1, miR-132 and SOX2 were determined by qRT-PCR and western blot. Proliferation of glioma cells was detected by MTT assay, while migration and invasion were determined by transwell assay. The target relationships were predicted by miRcode algorithm, and confirmed by dual luciferase reporter gene assay.ResultsNEAT1 was up-regulated in glioma. Knockdown of NEAT1 inhibited glioma cells’ viability, migration and invasion. MiR-132 was down-regulated while SOX2 was up-regulated in glioma cells. NEAT1 negatively regulated the expression of miR-132 in glioma while miR-132 targeted SOX2 to down-regulate its expression.ConclusionNEAT1 promoted glioma development by promoting SOX2 expression through suppressing miR-132.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0849-2) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Knockdown of long non-coding RNA NEAT1 inhibits glioma cell migration and invasion via modulation of SOX2 targeted by miR-132

et al. 2018

View full text Add to dashboard Cite

show abstract

“…As a transcription factor, CREB can be either target for specific miRNAs or modulator for miRNAs expression. By using the luciferase reporter system and real time PCR, Geng and coworkers identified CREB and KLF as a functional upstream regulator of the tumor suppressor miR-132 in U87 and U251 astrocytoma cells [98]. On the contrary, CREB abrogation by miR-1224-5p and miR-200b suppresses glioma progression in preclinical models [99,100].…”

Section: Creb and Brain Cancermentioning

confidence: 99%

Targeting CREB in Cancer Therapy: A Key Candidate or One of Many? An Update

Sapio

Salzillo

Ragone

et al. 2020

Cancers

View full text Add to dashboard Cite

Intratumor heterogeneity (ITH) is considered the major disorienting factor in cancer treatment. As a result of stochastic genetic and epigenetic alterations, the appearance of a branched evolutionary shape confers tumor plasticity, causing relapse and unfavorable clinical prognosis. The growing evidence in cancer discovery presents to us “the great paradox” consisting of countless potential targets constantly discovered and a small number of candidates being effective in human patients. Among these, cyclic-AMP response element-binding protein (CREB) has been proposed as proto-oncogene supporting tumor initiation, progression and metastasis. Overexpression and hyperactivation of CREB are frequently observed in cancer, whereas genetic and pharmacological CREB downregulation affects proliferation and apoptosis. Notably, the present review is designed to investigate the feasibility of targeting CREB in cancer therapy. In particular, starting with the latest CREB evidence in cancer pathophysiology, we evaluate the advancement state of CREB inhibitor design, including the histone lysine demethylases JMJD3/UTX inhibitor GSKJ4 that we newly identified as a promising CREB modulator in leukemia cells. Moreover, an accurate analysis of strengths and weaknesses is also conducted to figure out whether CREB can actually represent a therapeutic candidate or just one of the innumerable preclinical cancer targets.

show abstract

“…Mechanistic explorations in this study revealed that NEDD4 enhances the binding ability of KLF8 to the miR-132 promoter region and represses expression of miR-132. The transcription factor KLF8 was highlighted in a previously conducted study to modulate the expression of miR-132, which plays an important role in the tumorigenesis of astrocytoma 14 . Prior evidence has documented that the modulation of the miR-132/Sox5 signaling pathway by circDOCK1 affects the migration potential of bladder cancer cells 27 .…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, KLF8 is a transcription factor in the Sp/KLF family and has a pivotal role in cancer metastasis by stimulating the proliferation and migratory ability of bladder cancer cells 13 . KLF8 has been confirmed as a transcription factor of microRNA-132 (miR-132), and KLF8 can modulate the expression of miR-132 to exert functions in astrocytoma 14 . In bladder cancer, overexpressed levels of miR-132 were shown to restrict the migratory and invasive capacities of tumor cells and play a suppressive role in metastasis 15 .…”

Section: Introductionmentioning

confidence: 99%

Oncogenic E3 ubiquitin ligase NEDD4 binds to KLF8 and regulates the microRNA-132/NRF2 axis in bladder cancer

Mao

Yang

et al. 2022

Exp Mol Med

View full text Add to dashboard Cite

The neuronally expressed developmentally downregulated 4 (NEDD4) gene encodes a ubiquitin ligase that targets the epithelial sodium channel for degradation and has been implicated in tumor growth in various cancers. Hence, in this study, we intended to characterize the functional relevance of the NEDD4-mediated Kruppel-like factor 8/microRNA-132/nuclear factor E2-related factor 2 (KLF8/miR-132/NRF2) axis in the development of bladder cancer. NEDD4 and KLF8 were overexpressed in bladder cancer tissues and were associated with poorer patient survival rates. In bladder cancer cells, NEDD4 intensified the stability and transcriptional activity of KLF8 through ubiquitination to augment cell viability and migratory ability. Our investigations revealed that NEDD4 promotes the binding of KLF8 to the miR-132 promoter region and inhibits the expression of miR-132. KLF8 inhibited the expression of miR-132 to augment the viability and migratory ability of bladder cancer cells. Furthermore, miR-132 downregulated the expression of NRF2 to restrict the viability and migratory ability of bladder cancer cells. In addition, in vivo findings verified that NEDD4 regulates the KLF8/miR-132/NRF2 axis by accelerating tumor growth and lung metastasis. In conclusion, this study highlights NEDD4 as a potential therapeutic target against tumor recurrence and metastasis in bladder cancer.

show abstract

MicroRNA-132 targets PEA-15 and suppresses the progression of astrocytoma in vitro

Cited by 8 publications

References 41 publications

Knockdown of long non-coding RNA NEAT1 inhibits glioma cell migration and invasion via modulation of SOX2 targeted by miR-132

Knockdown of long non-coding RNA NEAT1 inhibits glioma cell migration and invasion via modulation of SOX2 targeted by miR-132

Targeting CREB in Cancer Therapy: A Key Candidate or One of Many? An Update

Oncogenic E3 ubiquitin ligase NEDD4 binds to KLF8 and regulates the microRNA-132/NRF2 axis in bladder cancer

Contact Info

Product

Resources

About