Adenosine induces cell‐cycle arrest and apoptosis in androgen‐dependent and ‐independent prostate cancer cell lines, LNcap‐FGC‐10, DU‐145, and PC3

Aghaei, Mahmoud; Karami-Tehrani, Fatemeh; Panjehpour, Mojtaba; Salami, Siamak; Fallahian, Faranak

doi:10.1002/pros.21438

Cited by 56 publications

(52 citation statements)

References 66 publications

(79 reference statements)

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“…Panjehpour et al [16] demonstrated that in DU145 prostate cancer cells, the A 2B AR was the highest expressed and the A 3 AR was the lowest expressed (almost undetectable) among the four subtypes of ARs. The results from the present study are different from those of Aghaei et al [14], who reported a different AR expression pattern with the A 3 AR being highly expressed. Fishman et al [17] reported that the A 3 AR agonist IB-MECA at concentrations from 0.01 to 10 μM inhibited growth of PC-3 cells, but the expression profile of four ARs was not examined.…”

Section: Discussioncontrasting

confidence: 99%

“…The A 2B AR has been identified as one of several GPCRs expressed at a considerably high level in some cancer tissues including prostate cancer [5]. However, the role of the A 2B AR in prostate cancer has not been systematically investigated and reliably identified [13,14]. This was, at least, in part, because many previous studies utilized adenosine and analogs that acted nonselectively on the ARs [13,15] rather than selective A 2B AR agonists or antagonists or siRNA specific for the A 2B AR.…”

Section: Discussionmentioning

confidence: 99%

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A2B adenosine receptor blockade inhibits growth of prostate cancer cells

Wei

Costanzi

Balasubramanian

et al. 2013

Purinergic Signalling

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The role of the A 2B adenosine receptor (AR) in prostate cell death and growth was studied. The A 2B AR gene expression quantified by real-time quantitative RT-PCR and Western blot analysis was the highest among four AR subtypes (A 1 , A 2A , A 2B , and A 3 ) in all three commonly used prostate cancer cell lines, PC-3, DU145, and LNCaP. We explored the function of the A 2B AR using PC-3 cells as a model. The A 2B AR was visualized in PC-3 cells by laser confocal microscopy. The nonselective A 2B AR agonist NECA and the selective A 2B

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A2B adenosine receptor blockade inhibits growth of prostate cancer cells

Wei

Costanzi

Balasubramanian

et al. 2013

Purinergic Signalling

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“…Similar effects were shown in these three cell lines when they were treated by adenosine (16). Both groups of agonists were shown to induce apoptosis and promoted G 0 /G 1 cell-cycle arrest through p53, cyclin-dependent kinase 4 (CDK4)/cyclin D1-mediated pathways (15,16). An evaluation of purinergic action in lineage-related cells ranging from androgen-sensitive to castrate-resistant as far as we are aware has not been performed.…”

supporting

confidence: 61%

“…An A 3 agonist was shown to have dose-dependent antiproliferative effects on androgen-sensitive (LNCaP-FGC10) and androgen-independent (DU145 and PC-3) PCa cells (15). Similar effects were shown in these three cell lines when they were treated by adenosine (16). Both groups of agonists were shown to induce apoptosis and promoted G 0 /G 1 cell-cycle arrest through p53, cyclin-dependent kinase 4 (CDK4)/cyclin D1-mediated pathways (15,16).…”

mentioning

confidence: 72%

Purinergic Receptor Expression and Cellular Responses to Purinergic Agonists in Human Prostate Cancer Cells

Lertsuwan

Peters

Johnson

et al. 2017

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Extracellular nucleotides were first proposed as signaling molecules in 1972 (1). Signaling through purinergic receptors is ubiquitous due to the diversity of purine and pyrimidine ligands, the number of receptors and extracellular nucleotidases. Purinergic signaling has been shown to play a role in many pathways including neurotransmission (2), cell differentiation, hormone secretion, vasodilation, cell proliferation, wound healing and apoptosis (3). There are two distinct families of purinergic receptors: P1 receptors for adenosine and P2 receptors for ATP/ADP and UTP/UDP ligands. P2 receptors are further divided into ligand-gated ion channel receptors, P2X, and G protein-coupled receptor, P2Y, subfamilies. To date, four P1 receptors (A 1,2a,2b,3 ), seven P2X receptors (P2X 1-7 ) and eight P2Y receptors (P2Y 1,2,4,6,11-14 ) have been identified in mammalian cells (4). The adenosine receptor subtypes A 1 and A 3 downregulate the production of cAMP, while A 2a and A 2b subtypes up-regulate the production of cAMP. Activation of P2X receptors leads to an influx of cations from the extracellular space, while activation of P2Y receptors leads to either an elevation of intracellular Ca 2+ from endoplasmic reticulum stores or down-regulation of cAMP production depending on the specific subtype of P2Y receptor activated.Growth suppression by the P2 agonist, ATP, was demonstrated first by Rapaport in 1983 (5). Exogenous ATP was shown to suppress the growth of pancreatic and colon cancer by causing cell-cycle arrest in S-phase. To date, the anticancer activity of extracellular nucleotides has been investigated in many types of cancer, including leukemia, melanoma and non-melanoma skin cancer, colorectal cancer, lung cancer, cervical cancer, prostate cancer (PCa) and squamous cell skin cancer (6). These led to clinical trials in patients with colorectal and non-small cell lung cancer that showed promising results with limited side-effects (7-9).PCa is the most frequently diagnosed cancer in North American men and the second leading cause of cancerrelated death in American men. It was estimated that there would be approximately 180,890 new cases of PCa and 26,5120 related deaths in the United States alone in 2016 (10). Current standard treatments for advanced PCa include various hormonal therapies whose goal is the ablation of androgens and their action (11). Even though 70% to 80% of patients respond well to first-line treatment, most patients eventually develop castrate-resistant disease (CRPCa) (12). Novel therapy therefore is needed to eliminate both early and 529 Τhis article is freely accessible online.

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“…Cell viability was determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay as described previously [23,24]. The A-431 cells were seeded at 5 × 10 3 cells/well in 5% CO2 at 37°C in RPMI medium (containing 10% FBS, 100 units⁄ml penicillin and 100 μg ⁄ml streptomycin) in 96-well plates.…”

Section: Cell Viability Assay With Mtt Reductionmentioning

confidence: 99%

Dihydroartemisinin induces apoptosis in skin cancer cell line A-431 via ROS pathway

Aghaei¹

2012

iosrphr

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Abstract--Dihydroartemisinin (DHA) is a derivative of artemisinin that has been shown to inhibit cell growth and induce apoptosis in the several cancer cells via reactive oxygen species (ROS) formation. The present study was designed to understand the mechanism underlying Dihydroartemisinin-induced apoptosis in the A-431 human skin cancer cell line.MTT viability assay was used to study the cell proliferation effect of Dihydroartemisinin. Annexin V-FITC and reactive oxygen species (ROS) formation were assessed to detect apoptosis. Dihydroartemisinin significantly inhibited cell proliferation in a concentration-dependent manner in A-431 cell line. Dihydroartemisinin significantly induced apoptosis, which was determined by Annexin V-FITC staining. Moreover, increase of ROS formation was observed in response to Dihydroartemisinin treatment. The results of this study suggest that Dihydroartemisinin inhibited cell proletarian and induced apoptosis in skin cancer cells via ROS pathways. These data might suggest that Dihydroartemisinin could be used as an agent for the treatment of skin cancer.

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Adenosine induces cell‐cycle arrest and apoptosis in androgen‐dependent and ‐independent prostate cancer cell lines, LNcap‐FGC‐10, DU‐145, and PC3

Abstract: Our results suggest that adenosine induced apoptosis in prostate cancer cells via the mitochondrial pathway and is related to the adenosine receptors. These data might suggest that adenosine could be used as an agent for the treatment of prostate cancer.

Cited by 56 publications

References 66 publications

A2B adenosine receptor blockade inhibits growth of prostate cancer cells

A2B adenosine receptor blockade inhibits growth of prostate cancer cells

Purinergic Receptor Expression and Cellular Responses to Purinergic Agonists in Human Prostate Cancer Cells

Dihydroartemisinin induces apoptosis in skin cancer cell line A-431 via ROS pathway

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