ARID1A-dependent permissive chromatin accessibility licenses estrogen-receptor signaling to regulate circadian rhythms genes in endometrial cancer

Hu, Hanyang; Chen, Zhiguo; Ji, Lulu; Wang, Yanling; Yang, Mengzhen; Lai, Rujie; Zhong, Yu; Zhang, Xiaoli; Wang, Lin

doi:10.1016/j.canlet.2020.08.034

Cited by 7 publications

(3 citation statements)

References 40 publications

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“…Mechanistically, binding of estrogen to EREs leads to the dimerization of ER, which induces accessible chromatin and forms higher-order super enhancers that are pivotal to ER signaling. ER is positively related to active enhancers particularly in primary tumors, and tumors are effectively classified into molecular subtypes with their dynamics of chromatin accessibility and ER-dependent gene signature ( 68 ). Given that ARID1A binds within ER-bound enhancers and thereby regulates ER-dependent transcription, it has been suggested that the wild-type ARID1A expression is related to a better clinical outcome in ER+ breast cancer patients, where fulvestrant combined with ARID1A inhibitor could be promisingly used for ER+ breast cancer, whereas ARID1A inactivating mutations are enriched in treatment-resistant tumors and metastases (in total 12% of cases) and ARID1A inactivation is thereby considered to be a tumor-promoting event in ER+ breast cancer ( 69 – 72 ).…”

Section: Tumor Suppression By Arid1amentioning

confidence: 99%

The Role of ARID1A in Tumors: Tumor Initiation or Tumor Suppression?

Tang

2021

Front. Oncol.

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Genes encoding subunits of SWItch/Sucrose Non-Fermenting (SWI/SNF) chromatin remodeling complexes are collectively mutated in 20% of all human cancers, among which the AT-rich interacting domain−containing protein 1A (ARID1A, also known as BAF250a, B120, C1orf4, Osa1) that encodes protein ARID1A is the most frequently mutated, and mutations in ARID1A have been found in various types of cancer. ARID1A is thought to play a significant role both in tumor initiation and in tumor suppression, which is highly dependent upon context. Recent molecular mechanistic research has revealed that ARID1A participates in tumor progression through its effects on control of cell cycle, modulation of cellular functions such as EMT, and regulation of various signaling pathways. In this review, we synthesize a mechanistic understanding of the role of ARID1A in human tumor initiation as well as in tumor suppression and further discuss the implications of these new discoveries for potential cancer intervention. We also highlight the mechanisms by which mutations affecting the subunits in SWI/SNF complexes promote cancer.

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Section: Tumor Suppression By Arid1amentioning

confidence: 99%

The Role of ARID1A in Tumors: Tumor Initiation or Tumor Suppression?

Tang

2021

Front. Oncol.

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“…Cancer is one of the most frequent diseases associated with circadian disruption (Barbosa Vieira et al, 2021; Hu et al, 2020). It is certain that some proteins, as p21 and p27 proteins, are controlled by core circadian proteins, exhibit a circadian pattern, or interact with the core clock system (Yang et al, 2021).…”

Section: Circadian Rhythm Associated Diseasesmentioning

confidence: 99%

Circadian rhythm and disease: Relationship, new insights, and future perspectives

Neves

Albuquerque

Quintela

et al. 2022

Journal Cellular Physiology

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The circadian system is responsible for internal functions and regulation of the organism according to environmental cues (zeitgebers). Circadian rhythm dysregulation or chronodisruption has been associated with several diseases, from mental to autoimmune diseases, and with life quality change. Following this, some therapies have been developed to correct circadian misalignments, such as light therapy and chronobiotics. In this manuscript, we describe the circadian‐related diseases so far investigated, and studies reporting relevant data on this topic, evidencing this relationship, are included. Despite the actual limitations in published work, there is clear evidence of the correlation between circadian rhythm dysregulation and disease origin/development, and, in this way, clock‐related therapies emerge as great progress in the clinical field. Future improvements in such interventions can lead to the development of successful chronotherapy strategies, deeply contributing to enhanced therapeutic outcomes.

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“…Inactivation of YAP activity by verteporfin treatment suppressed cell proliferation and invasion and induced apoptosis in endometrial cancer cells ( Dasari et al, 2017 ). Hu et al showed that ARID1A (AT-rich interactive domain-containing protein 1A), a key subunit of SWI/SNF complex, recruits FOXA1 (Forkhead Box A1) and TEAD4 to regulate ER binding on circadian rhythm genes in ER-positive endometrial cancer ( Hu et al, 2020 ). The transcriptional complex of TEAD4 and AP-1 controls cell migration and invasion by regulating its downstream targets such as CDH2 (Cadherin 2) and MACF1 (Microtubule Actin Crosslinking Factor 1) in endometrial cancer and other cancers ( Liu X. et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

TEAD4 as an Oncogene and a Mitochondrial Modulator

Hsu

Lin

et al. 2022

Front. Cell Dev. Biol.

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TEAD4 (TEA Domain Transcription Factor 4) is well recognized as the DNA-anchor protein of YAP transcription complex, which is modulated by Hippo, a highly conserved pathway in Metazoa that controls organ size through regulating cell proliferation and apoptosis. To acquire full transcriptional activity, TEAD4 requires co-activator, YAP (Yes-associated protein) or its homolog TAZ (transcriptional coactivator with PDZ-binding motif) the signaling hub that relays the extracellular stimuli to the transcription of target genes. Growing evidence suggests that TEAD4 also exerts its function in a YAP-independent manner through other signal pathways. Although TEAD4 plays an essential role in determining that differentiation fate of the blastocyst, it also promotes tumorigenesis by enhancing metastasis, cancer stemness, and drug resistance. Upregulation of TEAD4 has been reported in several cancers, including colon cancer, gastric cancer, breast cancer, and prostate cancer and serves as a valuable prognostic marker. Recent studies show that TEAD4, but not other members of the TEAD family, engages in regulating mitochondrial dynamics and cell metabolism by modulating the expression of mitochondrial- and nuclear-encoded electron transport chain genes. TEAD4’s functions including oncogenic activities are tightly controlled by its subcellular localization. As a predominantly nuclear protein, its cytoplasmic translocation is triggered by several signals, such as osmotic stress, cell confluency, and arginine availability. Intriguingly, TEAD4 is also localized in mitochondria, although the translocation mechanism remains unclear. In this report, we describe the current understanding of TEAD4 as an oncogene, epigenetic regulator and mitochondrial modulator. The contributing mechanisms will be discussed.

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ARID1A-dependent permissive chromatin accessibility licenses estrogen-receptor signaling to regulate circadian rhythms genes in endometrial cancer

Cited by 7 publications

References 40 publications

The Role of ARID1A in Tumors: Tumor Initiation or Tumor Suppression?

The Role of ARID1A in Tumors: Tumor Initiation or Tumor Suppression?

Circadian rhythm and disease: Relationship, new insights, and future perspectives

TEAD4 as an Oncogene and a Mitochondrial Modulator

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