Adenosine A1 receptor, a target and regulator of estrogen receptorα action, mediates the proliferative effects of estradiol in breast cancer

Lin, Zhihong; Yin, Ping; Reierstad, Scott; O'Halloran, Meghan; Coon, John S.; Pearson, E.; Mutlu, Gökhan M.; Bulun, Serdar E.

doi:10.1038/onc.2009.409

Cited by 58 publications

(43 citation statements)

References 41 publications

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“…These effects could be partially inhibited by using A1R antagonist. In contrast, a study by Lin et al [13] showed that A1R antagonist reduced proliferation in MCF-7 cells. Furthermore, knockdown of A1R by siRNA decreased cell proliferation, but over-expression of A1R could increase cell proliferation.…”

Section: Introductionmentioning

confidence: 73%

“…It has been documented that the A1R agonist could inhibit cell proliferation in colonic cancer, astrocytoma and melanoma cells [9, 10, 17]. In contrast, several studies also showed that the A1R antagonists could reduce cell proliferation [13, 18]. Notably, a combined treatment with A1R agonist and temozolomide significantly inhibited cell proliferation and promoted apoptosis compared to temozolomide alone in cancer stem cells [19], whereas A1R antagonist DPCPX was found to significantly induce apoptosis in MCF-7 cells [18].…”

Section: Discussionmentioning

confidence: 99%

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The Adenosine A1 Receptor Antagonist DPCPX Inhibits Tumor Progression via the ERK/JNK Pathway in Renal Cell Carcinoma

Zhou¹,

Tong²,

Chu³

et al. 2017

Cell Physiol Biochem

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Background/Aims: The adenosine A1 receptor (A1R) has been reported to be involved in the pathogenesis of various cancers, and the effects of A1R on different cancers are pleiotropic. However, the role of A1R in renal cell carcinoma (RCC) remains not well-known. Methods: The expression of A1R in RCC cells was detected by quantitative real-time PCR and Western blotting analysis. Cell proliferation was detected using an MTT assay and a colony formation assay. Tumor growth was also evaluated in nude mice. Cell invasion and migration were evaluated using a wound healing assay and a transwell assay. Cell cycle distribution and apoptosis rates were analyzed by flow cytometry. Results: A1R was the main subtype of ARs and was up-regulated in 786-O and ACHN cells. Functionally, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), an A1R antagonist, inhibited RCC cell proliferation in vitro and tumor growth in vivo. Furthermore, DPCPX inhibited RCC cell migration, while N⁶-Cyclopentyladenosine (CPA), a selective A1 agonist, was able to rescue RCC cell migration. In addition, DPCPX promoted 786-O and ACHN cell apoptosis and induced an S phase cell cycle arrest. Finally, we demonstrated that DPCPX inhibited tumor progression in part via the ERK/JNK pathway. Conclusion: These findings suggest the potentially important role of DPCPX in the control of RCC cell proliferation and migration by regulating the ERK/JNK signaling pathway.

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Section: Introductionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

The Adenosine A1 Receptor Antagonist DPCPX Inhibits Tumor Progression via the ERK/JNK Pathway in Renal Cell Carcinoma

Zhou¹,

Tong²,

Chu³

et al. 2017

Cell Physiol Biochem

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“…Not surprisingly, adenosine is appreciated for its complex role in many nervous system disorders such as alcoholism, epilepsy, traumatic brain injury, ischemia, anxiety, Alzheimer’s disease, Parkinson’s, and brain cancer [2,3,4,5,6,7,8]. Although progress has been made in understanding adenosine’s role in certain pain states, less is known about how it is involved in migraine [9].…”

Section: Introductionmentioning

confidence: 99%

The Role of Adenosine Signaling in Headache: A Review

2017

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Migraine is the third most prevalent disease on the planet, yet our understanding of its mechanisms and pathophysiology is surprisingly incomplete. Recent studies have built upon decades of evidence that adenosine, a purine nucleoside that can act as a neuromodulator, is involved in pain transmission and sensitization. Clinical evidence and rodent studies have suggested that adenosine signaling also plays a critical role in migraine headache. This is further supported by the widespread use of caffeine, an adenosine receptor antagonist, in several headache treatments. In this review, we highlight evidence that supports the involvement of adenosine signaling in different forms of headache, headache triggers, and basic headache physiology. This evidence supports adenosine A2A receptors as a critical adenosine receptor subtype involved in headache pain. Adenosine A2A receptor signaling may contribute to headache via the modulation of intracellular Cyclic adenosine monophosphate (cAMP) production or 5' AMP-activated protein kinase (AMPK) activity in neurons and glia to affect glutamatergic synaptic transmission within the brainstem. This evidence supports the further study of adenosine signaling in headache and potentially illuminates it as a novel therapeutic target for migraine.

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“…The activation of A1 adenosine receptors may thus contribute to resistance against trastuzumab (Herceptin) therapy, which relies on p27 upregulation (Lane et al, 2001). A1 adenosine receptor has also recently been shown to act as a target and regulator of estrogen receptor-a in breast cancer cells (Lin et al, 2010).…”

Section: Purinergic Signaling In Cancermentioning

confidence: 99%

Extracellular adenosine triphosphate and adenosine in cancer

2010

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Adenosine triphosphate (ATP) is actively released in the extracellular environment in response to tissue damage and cellular stress. Through the activation of P2X and P2Y receptors, extracellular ATP enhances tissue repair, promotes the recruitment of immune phagocytes and dendritic cells, and acts as a co-activator of NLR family, pyrin domain-containing 3 (NLRP3) inflammasomes. The conversion of extracellular ATP to adenosine, in contrast, essentially through the enzymatic activity of the ecto-nucleotidases CD39 and CD73, acts as a negativefeedback mechanism to prevent excessive immune responses. Here we review the effects of extracellular ATP and adenosine on tumorigenesis. First, we summarize the functions of extracellular ATP and adenosine in the context of tumor immunity. Second, we present an overview of the immunosuppressive and pro-angiogenic effects of extracellular adenosine. Third, we present experimental evidence that extracellular ATP and adenosine receptors are expressed by tumor cells and enhance tumor growth. Finally, we discuss recent studies, including our own work, which suggest that therapeutic approaches that promote ATP-mediated activation of inflammasomes, or inhibit the accumulation of tumorderived extracellular adenosine, may constitute effective new means to induce anticancer activity.

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Adenosine A1 receptor, a target and regulator of estrogen receptorα action, mediates the proliferative effects of estradiol in breast cancer

Cited by 58 publications

References 41 publications

The Adenosine A1 Receptor Antagonist DPCPX Inhibits Tumor Progression via the ERK/JNK Pathway in Renal Cell Carcinoma

The Adenosine A1 Receptor Antagonist DPCPX Inhibits Tumor Progression via the ERK/JNK Pathway in Renal Cell Carcinoma

The Role of Adenosine Signaling in Headache: A Review

Extracellular adenosine triphosphate and adenosine in cancer

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