ARID1A and CEBPα cooperatively inhibit UCA1 transcription in breast cancer

Guo, Xiao; Zhang, Yin; Mayakonda, Anand; Madan, Vikas; Ding, Ling-Wen; Lin, Le Hang; Zia, Saadiya; Gery, Sigal; Tyner, Jeffrey W.; Weiyuan, Zhou; Ding, Yin; Lin, De; Koeffler, H. Phillip

doi:10.1038/s41388-018-0371-4

Cited by 24 publications

(16 citation statements)

References 35 publications

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“…1). ARID1A plays a role as a transcriptional repressor in breast cancer (Guo et al, 2018). Loss of ARID1A profoundly alters histone modifications and the transcriptome.…”

Section: Discussionmentioning

confidence: 99%

Proline-Rich Acidic Protein 1 (PRAP1) is a Target of ARID1A and PGR in the Murine Uterus

Kim¹,

Jeong²

2019

Dev. Reprod.

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ARID1A and PGR plays an important role in embryo implantation and decidualization during early pregnancy. Uterine specific Arid1a knockout (Pgrcre/+Arid1af/f) mice exhibit in non-receptive endometrium at day 3.5 of gestation (GD 3.5). In previous studies, using transcriptomic analysis in the uterus of Pgrcre/+Arid1af/f mice, we identified proline-rich acidic protein 1 (PRAP1) as one of the down-regulated genes by ARID1A in the uterus. In the present study, we performed RT-qPCR and immunohistochemistry analysis to investigate the regulation of PRAP1 by ARID1A and determine expression patterns of PRAP1 in the uterus during early pregnancy. During early pregnancy, PRAP1 expression was strong at day 0.5 of gestation (GD 0.5) and then decreased at GD 3.5 in the epithelium and stroma. After implantation, PRAP1 expression was remarkably reduced in the uterus. However, the expression of PRAP1 at GD 3.5 was remarkably increased in the Pgrcre/+Arid1a f/f mice. To determine the ovarian steroid hormone regulation of PRAP1, we examined the expression of PRAP1 in ovariectomized control, Pgrcre/+Arid1af/f, and progesterone receptor knock-out (PRKO) mice treated with progesterone. While PRAP1 proteins were strongly expressed in the luminal and glandular epithelium of control mice treated with vehicle, progesterone treatment suppressed the expression of PRAP1. However, PRAP1 was not suppressed in both the Pgrcre/+Arid1af/f and PRKO mice compared to controls. Our results identified PRAP1 as a novel target of ARID1A and PGR in the murine uterus.

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“…1). ARID1A plays a role as a transcriptional repressor in breast cancer (Guo et al, 2018). Loss of ARID1A profoundly alters histone modifications and the transcriptome.…”

Section: Discussionmentioning

confidence: 99%

Proline-Rich Acidic Protein 1 (PRAP1) is a Target of ARID1A and PGR in the Murine Uterus

Kim¹,

Jeong²

2019

Dev. Reprod.

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“…UCA1 expression is regulated by several factors, such as transcription factors, chromatin remodeling and epigenetic modification (Fig. 2) (29)(30)(31). Furthermore, UCA1 contains microRNA (miRNA/miR) binding sites that regulate the expression of target genes through the sponging of miRNAs (Table I) (8,11,24).…”

Section: Overview Of Uca1mentioning

confidence: 99%

“…AT-rich interaction domain 1A (ARID1A) is one of the major members of SWItch/Sucrose non-fermentable chromatin remodeling complexes, which is often found to be loss-of-function mutations in different types of cancer, such as non-small cell lung cancer (NSCLC) (40), breast cancer (BC) (41) and pancreatic ductal adenocarcinoma (PDAC) (42). ARID1A inhibits UCA1 expression by regulating chromatin access of transcription factor C/EBPα (30). It has been confirmed that the CAPERα/TBX3 complex directly inhibits UCA1 transcription and promotes cancer cell senescence by regulating chromatin structure (43).…”

Section: Upstream Regulation Of Uca1 Expressionmentioning

confidence: 99%

Regulatory role of long non‑coding RNA UCA1 in signaling pathways and its clinical applications (Review)

et al. 2021

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Long non-coding RNA metastasis-associated urothelial carcinoma associated 1 (UCA1) plays a pivotal role in various human diseases. Its gene expression is regulated by several factors, including transcription factors, chromatin remodeling and epigenetic modification. UCA1 is involved in the regulation of the PI3K/AKT, Wnt/β-catenin, MAPK, NF-κB and JAK/STAT signaling pathways, affecting a series of cellular biological functions, such as cell proliferation, apoptosis, migration, invasion and tumor drug resistance. Furthermore, UCA1 is used as a novel potential biomarker for disease diagnosis and prognosis, as well as a target for clinical gene therapy. The present review systematically summarizes and elucidates the mechanisms of upstream transcriptional regulation of UCA1, the regulatory role of UCA1 in multiple signaling pathways in the occurrence and development of several diseases, and its potential applications in clinical treatment. Contents1. Introduction 2. Overview of UCA1 3. Upstream regulation of UCA1 expression 4. Signaling pathways regulated by UCA1 5. Clinical applications of UCA1 6. Conclusions and perspective

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“…For example, the lncRNA Low Expression in Tumor (LET) is transcriptionally silenced in various solid cancers by H istone Deacetylase 3 (HDAC3) -mediated promoter inactivation (79). Also, the lncRNA Urothelial Cancer Associated 1 (UCA1) is regulated by ARID1A, a component of the SWI/SNF chromatin-remodeling complex (80), and itself interacts with multiple histone-modifying proteins to regulate target gene expression (81).…”

Section: Lncrnas Can Act As Epigenetic Drivers In Human Cancermentioning

confidence: 99%

Long Non-coding RNAs as Functional and Structural Chromatin Modulators in Acute Myeloid Leukemia

Wurm

Pina

2019

Front. Oncol.

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Acute myeloid leukemia is a hematopoietic neoplasm of dismal prognosis that results from the accumulation of immature myeloid blasts in the bone marrow and the peripheral blood. It is strongly dependent on epigenetic regulation for disease onset, maintenance and in response to treatment. Epigenetic regulation refers to the multiple chemical modifications of DNA or DNA-associated proteins that alter chromatin structure and DNA accessibility in a heritable manner, without changing DNA sequence. Unlike sequence-specific transcription factors, epigenetic regulators do not necessarily bind DNA at consensus sequences, but still achieve reproducible target binding in a manner that is cell and maturation-type specific. A growing body of evidence indicates that epigenetic regulators rely, amongst other factors, on their interaction with untranslated RNA molecules for guidance to particular targets on DNA. Non (protein)-coding RNAs are the most abundant transcriptional products of the coding genome, and comprise several different classes of molecules with unique lengths, conformations and targets. Amongst these, long non-coding RNAs (lncRNAs) are species of 200 bp to >100 K bp in length, that recognize, and bind unique and largely uncharacterized DNA conformations. Some have been shown to bind epigenetic regulators, and thus constitute attractive candidates to mediate epigenetic target specificity. Herein, we postulate that lncRNAs are central players in the unique epigenetic programming of AML and review recent evidence in support of this view. We discuss the value of lncRNAs as putative diagnostic, prognostic and therapeutic targets in myeloid leukemias and indicate novel directions in this exciting research field.

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ARID1A and CEBPα cooperatively inhibit UCA1 transcription in breast cancer

Cited by 24 publications

References 35 publications

Proline-Rich Acidic Protein 1 (PRAP1) is a Target of ARID1A and PGR in the Murine Uterus

Proline-Rich Acidic Protein 1 (PRAP1) is a Target of ARID1A and PGR in the Murine Uterus

Regulatory role of long non‑coding RNA UCA1 in signaling pathways and its clinical applications (Review)

Long Non-coding RNAs as Functional and Structural Chromatin Modulators in Acute Myeloid Leukemia

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