A p53/CPEB2 negative feedback loop regulates renal cancer cell proliferation and migration

Di, Jiehui; Zhao, Guang Yu; Wang, Hui; Wu, Yaoyao; Zhao, Zhongjun; Zhu, Bao Ting; Zhang, Yanping; Zheng, Junnian; Liu, Yong; Hu, Ying

doi:10.1016/j.jgg.2021.05.011

Cited by 10 publications

(4 citation statements)

References 35 publications

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“…S4 G ). Correlated with this, it has been recently reported that as a transcriptional target of p53, CPEB2 is up-regulated by p53 ( 67 ). Together, these findings imply that the posttranscriptional regulation of p53 by the EMS–CPEB2 axis could be a common feature in p53 wild-type LUAD.…”

Section: Discussionmentioning

confidence: 72%

Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis

Wang

Yang

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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p53 plays a central role in tumor suppression. Emerging evidence suggests long noncoding RNA (lncRNA) as an important class of regulatory molecules that control the p53 signaling. Here, we report that the oncogenic lncRNA E2F1 messenger RNA (mRNA) stabilizing factor (EMS) and p53 mutually repress each other’s expression. EMS is negatively regulated by p53. As a direct transcriptional repression target of p53, EMS is surprisingly shown to inhibit p53 expression. EMS associates with cytoplasmic polyadenylation element-binding protein 2 (CPEB2) and thus, disrupts the CPEB2–p53 mRNA interaction. This disassociation attenuates CPEB2-mediated p53 mRNA polyadenylation and suppresses p53 translation. Functionally, EMS is able to exert its oncogenic activities, at least partially, via the CPEB2–p53 axis. Together, these findings reveal a double-negative feedback loop between p53 and EMS, through which p53 is finely controlled. Our study also demonstrates a critical role for EMS in promoting tumorigenesis via the negative regulation of p53.

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Section: Discussionmentioning

confidence: 72%

Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis

Wang

Yang

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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“… 66 At 4p15.33, we prioritized the translational regulatory factor CPEB2 , 67 which is known to promote senescence and suppress epithelial-to-mesenchymal transition by regulating p53, HIF1α, and Twist1 translation. 68 , 69 Knockdown of CPEB in vitro caused p53 protein levels to decrease by 50%. 70 The risk variants at this locus were cis -eQTLs, downregulating CPEB2 expression ( Supplementary Table S8 , available at https://doi.org/10.1016/j.annonc.2024.02.008 ).…”

Section: Resultsmentioning

confidence: 99%

Genome-wide association studies and Mendelian randomization analyses provide insights into the causes of early-onset colorectal cancer

Laskar,

Qu,

Huyghe

et al. 2024

Annals of Oncology

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“…CPEB1 upregulates the polyadenylation-induced translation of p53 mRNA in primary human cells ( Burns and Richter, 2008 ). In addition, our recently published study ( Di et al, 2021 ) showed that CPEB2, as a target of p53, can regulate p53 via a negative feedback mechanism. Therefore, CPEB family proteins may have different functions in regulating p53.…”

Section: Discussionmentioning

confidence: 98%

CPEB4 Inhibit Cell Proliferation via Upregulating p21 mRNA Stability in Renal Cell Carcinoma

Wang

Zhao

et al. 2021

Front. Cell Dev. Biol.

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Cytoplasmic polyadenylation element-binding protein 4 (CPEB4) has been reported to be dysregulated in a variety of cancers and seems to play paradoxical roles in different cancers. However, the functional roles of CPEB4 in Renal cell carcinoma (RCC) are still unclear. This study aims to explore the role and underlying mechanism of CPEB4 in RCC. We found that the relative expression level of CPEB4 is down-regulated in RCC tissues and cell lines, and the low CPEB4 expression is correlated with short overall and disease-free survival of RCC patients. CPEB4 significantly inhibits RCC tumor growth both in vivo and in vitro. CPEB4 exerts an anti-tumor effect by increasing p21 mRNA stability and inducing G1 cell cycle arrest in RCC. Our data revealed that CPEB4 is a tumor suppressor gene that restrains cell cycle progression upstream of p21 in RCC. These findings revealed that CPEB4 may become a promising predictive biomarker for prognosis in patients with RCC.

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A p53/CPEB2 negative feedback loop regulates renal cancer cell proliferation and migration

Cited by 10 publications

References 35 publications

Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis

Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis

Genome-wide association studies and Mendelian randomization analyses provide insights into the causes of early-onset colorectal cancer

CPEB4 Inhibit Cell Proliferation via Upregulating p21 mRNA Stability in Renal Cell Carcinoma

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