The role of the transcription factor Ets1 in carcinoma

Dittmer, Jürgen

doi:10.1016/j.semcancer.2015.09.010

Cited by 174 publications

(194 citation statements)

References 303 publications

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“…ETS1 overexpression is also found in human breast cancer (BC) associated with invasiveness and poor prognosis (87, 88). By overexpressing Ets1 or a dominant-negative mutant in BC cells, it was shown that ETS1 plays a key role in coordinating multiple invasive features of cancer cells (87).…”

Section: Ets1 and Ets2mentioning

confidence: 99%

Aberrant expression of ETS1 and ETS2 proteins in cancer

Fry

Inoue

2018

Cancer Rep Rev

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The ETS transcription factors regulate expression of genes involved in normal cell development, proliferation, differentiation, angiogenesis, and apoptosis, consisting of 28 family members in humans. Dysregulation of these transcription factors facilitates cell proliferation in cancers, and several members participate in invasion and metastasis by activating gene transcription. ETS1 and ETS2 are the founding members of the ETS family and regulate transcription by binding to ETS sequences. They are both involved in oncogenesis and tumor suppression depending on the biological situations used. The essential roles of ETS proteins in human telomere maintenance have been suggested, which have been linked to creation of new Ets binding sites. Recently, preferential binding of ETS2 to gain-of-function mutant p53 and ETS1 to wild type p53 (WTp53) has been suggested, raising the tumor promoting role for the former and tumor suppressive role for the latter. The oncogenic and tumor suppressive functions of ETS1 and 2 proteins have been discussed.

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Section: Ets1 and Ets2mentioning

confidence: 99%

Aberrant expression of ETS1 and ETS2 proteins in cancer

Fry

Inoue

2018

Cancer Rep Rev

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“…Ets factors do not only participate in hematopoiesis (Ciau-Uitz et al, 2013) but also have a role in normal development and pathology of cardiovascular and endocrine systems (Dittmer, 2015;Gutierrez-Hartmann et al, 2007;Meadows et al, 2011); this might, at least in part, explain the TESC-associated conditions affecting the CNS and other organs (see below). Tescalcin is also involved in the differentiation and maturation of granulocytes, a process that is also mediated by ERK1/2 signaling (Levay and Slepak, 2010).…”

Section: Subcellular Localization and Tissue Distribution Of Tescalcinmentioning

confidence: 99%

Emerging roles of the single EF-hand Ca2+ sensor tescalcin in the regulation of gene expression, cell growth and differentiation

Kolobynina

Solovyova

Levay

et al. 2016

Journal of Cell Science

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Tescalcin (TESC, also known as calcineurin-homologous protein 3, CHP3) is a 24-kDa EF-hand Ca2+-binding protein that has recently emerged as a regulator of cell differentiation and growth. The TESC gene has also been linked to human brain abnormalities, and high expression of tescalcin has been found in several cancers. The expression level of tescalcin changes dramatically during development and upon signal-induced cell differentiation. Recent studies have shown that tescalcin is not only subjected to up- or down-regulation, but also has an active role in pathways that drive cell growth and differentiation programs. At the molecular level, there is compelling experimental evidence showing that tescalcin can directly interact with and regulate the activities of the Na+/H+ exchanger NHE1, subunit 4 of the COP9 signalosome (CSN4) and protein kinase glycogen-synthase kinase 3 (GSK3). In hematopoetic precursor cells, tescalcin has been shown to couple activation of the extracellular signal-regulated kinase (ERK) cascade to the expression of transcription factors that control cell differentiation. The purpose of this Commentary is to summarize recent efforts that have served to characterize the biochemical, genetic and physiological attributes of tescalcin, and its unique role in the regulation of various cellular functions.

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“…Since first indentified as the cellular proto-oncogene of retroviral v-ETS [22], a series of studies have demonstrated that Ets-1 regulates transcription through recognizing binding sites within gene promoters, and participates in many biological processes, such as cellular differentiation, proliferation, transformation, angiogenesis, and cancer progression [9]. Ets-1 facilitates cell cycle G1/S progression and cellular proliferation via up-regulating cyclin E and cyclin dependent kinase 2 [23].…”

Section: Discussionmentioning

confidence: 99%

“…V-ets erythroblastosis virus E26 oncogene homolog 1 ( Ets-1 ), one transcription factor of E26 transformation-specific (Ets) family, is upregulated in many solid tumors, such as breast [3], cervical [4], colorectal [5], lung [6], and ovarian [7, 8] cancers, which is associated with tumor angiogenesis and lymph node or distant metastasis [9]. Ets-1 promotes the growth and metastasis of different cancer cell lines [9], while knockdown of Ets-1 inhibits cell transformation [10] and reverses the multiple drug resistance of breast cancer cells [11]. Our previous evidence shows that Ets-1 levels are elevated in gastric cancer, and knockdown of Ets-1 inhibits the invasiveness and metastasis of gastric cancer cells [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Ets-1 promoter-associated noncoding RNA regulates the NONO/ERG/Ets-1 axis to drive gastric cancer progression

Chen

Hong

et al. 2018

Oncogene

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Emerging studies have indicated the essential functions of long noncoding RNAs (lncRNAs) during cancer progression. However, whether lncRNAs contribute to the upregulation of v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets-1), an established oncogenic protein facilitating tumor invasion and metastasis, in gastric cancer remains elusive. Herein, we identified Ets-1 promoter-associated noncoding RNA (pancEts-1) as a novel lncRNA associated with the gastric cancer progression via mining of publicly available datasets and rapid amplification of cDNA ends. RNA pull-down, RNA immunoprecipitation, in vitro binding, and RNA electrophoretic mobility shift assays indicated the binding of pancEts-1 to non-POU domain containing octamer binding (NONO) protein. Mechanistically, pancEts-1 facilitated the physical interaction between NONO and Ets related gene (ERG), resulting in increased ERG transactivation and transcription of Ets-1 associated with gastric cancer progression. In addition, pancEts-1 facilitated the growth and aggressiveness of gastric cancer cells via interacting with NONO. In gastric cancer tissues, pancEts-1, NONO, and ERG were upregulated and significantly correlated with Ets-1 levels. High levels of pancEts-1, NONO, ERG, or Ets-1 were respectively associated with poor survival of gastric cancer patients, whereas simultaneous expression of all of them (HR = 3.012, P = 0.105) was not an independent prognostic factor for predicting clinical outcome. Overall, these results demonstrate that lncRNA pancEts-1 exhibits oncogenic properties that drive the progression of gastric cancer via regulating the NONO/ERG/Ets-1 axis.

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The role of the transcription factor Ets1 in carcinoma

Cited by 174 publications

References 303 publications

Aberrant expression of ETS1 and ETS2 proteins in cancer

Aberrant expression of ETS1 and ETS2 proteins in cancer

Emerging roles of the single EF-hand Ca2+ sensor tescalcin in the regulation of gene expression, cell growth and differentiation

Ets-1 promoter-associated noncoding RNA regulates the NONO/ERG/Ets-1 axis to drive gastric cancer progression

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