Tristetraprolin Represses Estrogen Receptor α Transactivation in Breast Cancer Cells

Barrios-García, Tonatiuh; Tecalco-Cruz, Ángeles C.; Gómez-Romero, Vania; Reyes-Carmona, Sandra; Meneses-Morales, Iván; León-Del-Río, Alfonso

doi:10.1074/jbc.m114.548552

Cited by 18 publications

(31 citation statements)

References 55 publications

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“…Most of the previous studies of TTP have focused mainly on the functions of TTP in breast tumor progression (Barrios-Garcia et al, 2014;Milke et al, 2013;Pandiri et al, 2016). The regulatory signaling factors that directly regulate TTP are not fully defined.…”

Section: Pim2 Interacts With Ttpmentioning

confidence: 99%

PIM2 interacts with tristetraprolin and promotes breast cancer tumorigenesis

et al. 2018

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Tristetraprolin (TTP) is an AU‐rich element‐binding protein that regulates mRNA stability and plays important roles in cancer. The mechanisms by which TTP is regulated in breast cancer are poorly understood. Using multiple biochemical approaches, we found that proviral insertion in murine lymphomas 2 (PIM2) is a novel binding partner of TTP. Interestingly, PIM2 decreased TTP protein levels independent of its kinase activity. PIM2 instead targeted TTP protein for degradation via the ubiquitin‐proteasome pathway. Furthermore, immunohistochemical staining showed that PIM2 and TTP protein levels were negatively correlated in human breast cancer samples. Indeed, PIM2 overexpression de‐repressed TTP‐mediated inhibition of breast cancer cell proliferation and migration in vitro and promoted breast tumor xenograft growth in vivo. These findings demonstrate an important role for the PIM2‐TTP complex in breast cancer tumorigenesis, suggesting that PIM2 may represent a potential therapeutic target for breast cancer treatment.

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Section: Pim2 Interacts With Ttpmentioning

confidence: 99%

PIM2 interacts with tristetraprolin and promotes breast cancer tumorigenesis

et al. 2018

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“…ZFP36 was a downregulated gene in BC, and upregulation of ZFP36 inhibited transactivation of ERα, cell proliferation, as well as the capacity to form new tumors 18,30 . It was noted that circRNAs played critical functions during tumor progression by binding to miRs and miRs affected behaviors of malignant cells by regulating posttranscriptional gene expression 11,31 .…”

Section: Discussionmentioning

confidence: 99%

Circular RNA 000554 represses epithelial‐mesenchymal transition in breast cancer by regulating microRNA‐182/ZFP36 axis

Mao

Cao

et al. 2020

FASEB j.

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Increasing evidence indicates that circular RNAs (circRNAs) play a crucial role in regulating microRNAs (miRs) and mRNAs during breast cancer (BC) progression. Based on the in silico analysis of circRNA/miR/mRNA in BC, we aim to define an important role of circRNA_000554 in BC in relation to miR‐182 and zinc finger protein 36 (ZFP36). Low expression of circRNA_000554 and ZFP36, and high miR‐182 expression were determined in the clinical BC tissues. CircRNA_000554 acted as a sponge of miR‐182, and miR‐182 directly targeted ZFP36. After that, in order to evaluate the effects of circRNA_000554, miR‐182, and ZFP36 on cellular process, we evaluated in vitro epithelial‐mesenchymal transition (EMT) and in vivo tumor growth after delivering a series of overexpression plasmids, mimic, inhibitor, or shRNAs into BC cells. Increasing circRNA_000554 suppressed EMT, cell invasion and migration during BC by depleting miR‐182 and increasing ZFP36. The inhibitory effect of circRNA_000554 on tumor growth was validated in vivo. Taken together, the present study confirms that circRNA_000554 functioned as an inhibitor of EMT in BC and suggests a molecular mechanism that circRNA_000554 bound to miR‐182 to upregulate ZFP36 in this process.

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“…In ER − MDA-MB-231 cells, we didn't observe cell death after TTP being induced even for 6 days (data not shown). Barrios-Garcia et al recently reported that MCF7 cells overexpressing TTP exhibit a significant reduction in ERα-dependent transcriptional activation and in E2-induced cell proliferation [ 42 ]. This could be the reason why TTP induces stronger inhibition of cell proliferation, even cell death, in ER positive cells (MCF7) than in ER negative cells (MDA-MB-231).…”

Section: Discussionmentioning

confidence: 99%

Tristetraprolin induces cell cycle arrest in breast tumor cells through targeting AP-1/c-Jun and NF-κB pathway

Ning

et al. 2015

Oncotarget

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The main characteristic of cancers, including breast cancer, is the ability of cancer cells to proliferate uncontrollably. However, the underlying mechanisms of cancer cell proliferation, especially those regulated by the RNA binding protein tristetraprolin (TTP), are not completely understood. In this study, we found that TTP inhibits cell proliferation in vitro and suppresses tumor growth in vivo through inducing cell cycle arrest at the S phase. Our studies demonstrate that TTP inhibits c-Jun expression through the C-terminal Zn finger and therefore increases Wee1 expression, a regulatory molecule which controls cell cycle transition from the S to the G2 phase. In contrast to the well-known function of TTP in regulating mRNA stability, TTP inhibits c-Jun expression at the level of transcription by selectively blocking NF-κB p65 nuclear translocation. Reconstitution of NF-κB p65 completely abolishes the inhibition of c-Jun transcription by TTP. Moreover, reconstitution of c-Jun in TTP-expressing breast tumor cells diminishes Wee1 overexpression and promotes cell proliferation. Our results indicate that TTP suppresses c-Jun expression that results in Wee1 induction which causes cell cycle arrest at the S phase and inhibition of cell proliferation. Our study provides a new pathway for TTP function as a tumor suppressor which could be targeted in tumor treatment.

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Tristetraprolin Represses Estrogen Receptor α Transactivation in Breast Cancer Cells

Cited by 18 publications

References 55 publications

PIM2 interacts with tristetraprolin and promotes breast cancer tumorigenesis

PIM2 interacts with tristetraprolin and promotes breast cancer tumorigenesis

Circular RNA 000554 represses epithelial‐mesenchymal transition in breast cancer by regulating microRNA‐182/ZFP36 axis

Tristetraprolin induces cell cycle arrest in breast tumor cells through targeting AP-1/c-Jun and NF-κB pathway

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