Transcriptionally elevation of miR-494 by new ChlA-F compound via a HuR/JunB axis inhibits human bladder cancer cell invasion

Tian, Zhongxian; Luo, Yisi; Zhu, Junlan; Hua, Xiaohui; Xu, Jiheng; Huang, Chao; Jin, Honglei; Huang, Haishan; Huang, Chuanshu

doi:10.1016/j.bbagrm.2019.05.007

Cited by 5 publications

(3 citation statements)

References 49 publications

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“…This miRNA has been identified as an important factor and a promising therapeutic target for lung cancer 8 and muscle-invasive bladder cancer. 9 Moreover, miR-494 is highly expressed in hepatocellular carcinoma (HCC), it may be related to tumor size and stemness markers, and it is a possible therapeutic target and a candidate biomarker for stratification of patients with advanced HCC. 10 Propofol is an intravenous hypnotic agent used to induce and maintain sedation and general anesthesia, and it enhances the inhibitory neurotransmitter gammaaminobutyric acid at the gammaaminobutyric acid A receptor.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion injury

Zou

et al. 2021

J Int Med Res

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Objective This study aimed to investigate the effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion (I/R) injury. Methods Forty healthy adult male Sprague-Dawley rats were allocated to the sham operation group and three hepatic I/R injury groups. The I/R injury groups included I/R injury only (I/R group), treatment with propofol (propofol group), and treatment with propofol + overexpressed miR-494 (propofol+miR-494 group). Apoptosis of myocardial cells and changes in cardiac function indices, including left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and left ventricular posterior wall thickness, as well as changes in miR-494, were monitored. Results The apoptotic rate of myocardial cells in the I/R group was higher, cardiac function was deteriorated, and miR-494 levels were elevated compared with the sham group. The apoptotic rate was lower, cardiac function was improved, and miR-494 levels were suppressed in the propofol group compared with the I/R group. The apoptotic rate was higher, cardiac function was deteriorated, and miR-494 levels were elevated in the propofol+miR-494 group compared with the propofol group. Conclusion Propofol plays a vital role in preventing myocardial cell apoptosis and improvement of cardiac function by suppressing miR-494 in a hepatic I/R injury rat model.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion injury

Zou

et al. 2021

J Int Med Res

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“…HuR-miR-494. In muscle invasive bladder cancer (MIBC) cells (T24T), the anti-cancerous compound ChlA-F, a novel C8 fluoride derivative of cheliensisin A, increases JUNB mRNA stability in a HuR-dependent manner [ 134 ]. Then, Jun-B promotes miR-494 expression, which, in turn, directly binds and decreases c-Myc mRNA [ 134 ].…”

Section: Aubps Interfering With Mirnas-dependent Regulationmentioning

confidence: 99%

MicroRNAs, Tristetraprolin Family Members and HuR: A Complex Interplay Controlling Cancer-Related Processes

Sobolewski

Dubuquoy

Legrand

2022

Cancers

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MicroRNAs represent the most characterized post-transcriptional regulators of gene expression. Their altered expression importantly contributes to the development of a wide range of metabolic and inflammatory diseases but also cancers. Accordingly, a myriad of studies has suggested novel therapeutic approaches aiming at inhibiting or restoring the expression of miRNAs in human diseases. However, the influence of other trans-acting factors, such as long-noncoding RNAs or RNA-Binding-Proteins, which compete, interfere, or cooperate with miRNAs-dependent functions, indicate that this regulatory mechanism is much more complex than initially thought, thus questioning the current models considering individuals regulators. In this review, we discuss the interplay existing between miRNAs and the AU-Rich Element Binding Proteins (AUBPs), HuR and tristetraprolin family members (TTP, BRF1 and BRF2), which importantly control the fate of mRNA and whose alterations have also been associated with the development of a wide range of chronic disorders and cancers. Deciphering the interplay between these proteins and miRNAs represents an important challenge to fully characterize the post-transcriptional regulation of pro-tumorigenic processes and design new and efficient therapeutic approaches.

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“…A growing body of literature suggests that TP53 mutations in lung cancer are associated with increased resistance to cancer therapy and poorer survival prognosis (6), thus, mutp53 is a promising therapeutic target. Many natural or naturally derived antitumor drugs [curcumin (13), artemisinin (14), capsaicin (15)] have begun to play increasingly important roles in clinical cancer treatment (16).…”

Section: Introductionmentioning

confidence: 99%

Triptolide promotes degradation of the unfolded gain-of-function Tp53R175H/Y220C mutant protein by initiating heat shock protein 70 transcription in non-small cell lung cancer

Zhou

Luo

et al. 2022

Transl Lung Cancer Res

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Background: The mutation rate of the tumor protein P53 (TP53) has been reported to be greater than 50% in non-small cell lung cancer (NSCLC), and gain-of-function (GOF) mutations in unfolded P53 (TP53 R175H and TP53 Y220C ) have been associated with poor prognosis. However, the best treatment for patients with NSCLC harboring unfolded mutant P53 (mutp53) remains unclear. Triptolide is a natural compound derived from Tripterygium wilfordii that has shown a strong antitumor effect in a variety of cancers. Our study aimed to explore the GOF mutations in unfolded mutp53 (TP53 R175H and TP53 Y220C ) and to clarify the molecular mechanisms by which triptolide regulates the degradation of unfolded mutp53 proteins in NSCLC.Methods: Two unfolded proteins harboring TP53 R175H and TP53 Y220C mutations were selected to explore their functions in NSCLC progression. NCI-H1299 cells (TP53-null) were transfected with wild-type TP53 (TP53 WT ), TP53 R175H , or TP53 Y220C genes and treated with triptolide or a vehicle. Wound healing and transwell assays were performed to measure cell migration and invasion in vitro. Lung metastasis models were constructed through tail vein injection of mutant cells into BALB/c nude mice to evaluate the effect of triptolide on metastasis in vivo. Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), immunoprecipitation, and dual-luciferase reporter assays were performed to explore the relevant molecular mechanisms.Results: Our study revealed that triptolide treatment reduced TP53 R175H levels and that the TP53 Y220C mutation enhanced the invasion and migration of NCI-H1299 cells. Mechanistically, triptolide promoted TP53 R175H and TP53 Y220C protein proteasomal degradation mediated through the E3 ligase murine double minute 2 (MDM2) by directly interacting with heat shock protein 70 (HSP70). Moreover, by upregulating HSP70 transcription, triptolide contributed to the protein degradation of the GOF mutp53.Conclusions: Our study reports, for the first time, the mechanism underlying triptolide-regulated protein degradation of TP53 R175H or TP53 Y220C , which offers new insight into developing a better therapeutic strategy for patients with NSCLC who express the unfolded mutp53 GOF protein. Methods Cell lines, cell culture, and reagentsHuman lung epithelial NCI-H1299 (TP53-null)

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Transcriptionally elevation of miR-494 by new ChlA-F compound via a HuR/JunB axis inhibits human bladder cancer cell invasion

Cited by 5 publications

References 49 publications

RETRACTED: Effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion injury

RETRACTED: Effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion injury

MicroRNAs, Tristetraprolin Family Members and HuR: A Complex Interplay Controlling Cancer-Related Processes

Triptolide promotes degradation of the unfolded gain-of-function Tp53R175H/Y220C mutant protein by initiating heat shock protein 70 transcription in non-small cell lung cancer

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