The effect of adenosine A1 receptor agonist and antagonist on p53 and caspase 3, 8, and 9 expression and apoptosis rate in MCF-7 breast cancer cell line

Dastjerdi, Mehdi Nikbakht; Rarani, Mohammad Zamani; Valiani, Ali; Mahmoudieh, Mohsen

doi:10.4103/1735-5362.189301

Cited by 28 publications

(24 citation statements)

References 23 publications

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“…P53 is a tumor suppressor protein regulating cell cycle progression and apoptosis in tumor cells (Bordon, ; Maiuri et al, ). In line with this, Dastjerdi, Rarani, Valiani, and Mahmoudieh ( ) showed that upon addition of N6‐Cyclopentyladenosine (CPA), an A1 adenosine receptor agonist, viability rate of MCF‐7 cells increases and apoptosis reduces dramatically. Expression of P53 and caspases decrease as well.…”

Section: Role Of Adenosine In Apoptosis In Breast Cancermentioning

confidence: 73%

Role of adenosine signaling in the pathogenesis of breast cancer

Bahreyni

Samani

Rahmani

et al. 2017

Journal Cellular Physiology

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The plasma level of adenosine increases under ischemic and inflamed conditions in tumor microenvironment. Adenosine elicits a range of signaling pathways in tumors, resulting in either inhibition or enhancement of tumor growth depending upon different subtypes of adenosine receptors activation and type of cancer. Metabolism of adenosine-5'-triphosphate (ATP) and its derivatives including adenosine is dysregulated in the breast tumor microenvironment, supporting the role of this metabolite in the pathogenesis of breast cancer. Adenosine regulates inflammation, apoptosis, cell proliferation, and metastasis in breast cancer cells. This review summarizes the role of adenosine in the pathogenesis of breast cancer for a better understanding and hence a better management of this disease.

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Section: Role Of Adenosine In Apoptosis In Breast Cancermentioning

confidence: 73%

Role of adenosine signaling in the pathogenesis of breast cancer

Bahreyni

Samani

Rahmani

et al. 2017

Journal Cellular Physiology

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“…It has been demonstrated that the occurrence of tumor development depends on the dynamic balance between cell proliferation and apoptosis (23). Caspase-3 is a important apoptotic protein for various cells, and caspase-3 activation can induce apoptosis in cancer cells (24). The Bcl-2 family of apoptosis-related proteins includes important regulatory factors: Bcl-2 inhibits apoptosis, whereas Bax and Bak promote apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Naphthazarin suppresses cell proliferation and induces apoptosis in human colorectal cancer cells via the B-cell lymphoma 2/B-cell associated X protein signaling pathway

Chen

et al. 2016

Oncology Letters

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Abstract. Colorectal cancer is the most common gastrointestinal cancer in the USA. Naphthazarin, one of the naturally available 1,4-naphthoquinone derivatives, is a natural bioactive molecule that exhibits an antitumor effect. To the best of our knowledge, this is the first study to investigate the anticancer effect of naphthazarin on cell proliferation and apoptosis in human SW480 colorectal cancer cells. In the present study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were performed to assess the effect of napthazarin on cell proliferation and cytotoxicity of SW430 cells, respectively. In addition, an Annexin V-fluorescein isothiocyanate/propidium iodide apoptosis assay and 4' ,6-diamidino-2-phenylindole staining were used to analyze cell and nuclei apoptosis of SW480 cells, respectively, following treatment with naphthazarin. Poly (ADP-ribose) polymerase (PARP), B-cell lymphoma 2 (Bcl-2) and B-cell associated X protein (Bax) protein expression was analyzed by western blot. Furthermore, caspase-3 activation was analyzed using a commercial kit. The results revealed that naphthazarin exhibited cell growth inhibition, an increase in cytotoxicity and apoptosis induction in SW480 cells, which was associated with activation of the Bax/Bcl-2 signaling pathway and cleaved caspase-3 activation. However, no significant differences in PARP expression were identified following treatment with naphthazarin in SW480 cells. Taken together, these results suggest that naphthazarin decreased cell viability and induced apoptosis of SW480 cells, indicating that naphthazarin may present a potential therapeutic agent for human colorectal cancer treatment.

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“…These processes are likely to be related to PRODH/POX-dependent ROS signaling and subsequent activation of caspases or regulation by transcription factors. MCF-7 cells express wild-type p53 protein [ 28 ]. PRODH/POX expression is regulated by P53 [ 29 – 31 ], while PRODH/POX down regulates HIF-1α signaling [ 32 ], that mediate glycolysis, angiogenesis, metastasis and survival [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Proline oxidase silencing induces proline-dependent pro-survival pathways in MCF-7 cells

et al. 2018

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Proline degradation by proline dehydrogenase/proline oxidase (PRODH/POX) contributes to apoptosis or autophagy. The identification of specific pathway of apoptosis/survival regulation is the aim of this study. We generated knocked-down PRODH/POX MCF-7 breast cancer cells (MCF-7shPRODH/POX). PRODH/POX silencing did not affect cell viability. However, it contributed to decrease in DNA and collagen biosynthesis, increase in prolidase activity and intracellular proline concentration as well as increase in the expression of iNOS, NF-κB, mTOR, HIF-1α, COX-2, AMPK, Atg7 and Beclin-1 in MCF-7shPRODH/POX cells. In these cells, glycyl-proline (GlyPro, substrate for prolidase) further inhibited DNA and collagen biosynthesis, maintained high prolidase activity, intracellular concentration of proline and up-regulated HIF-1α, AMPK, Atg7 and Beclin-1, compared to GlyPro-treated MCF-7 cells. In MCF-7 cells, GlyPro increased collagen biosynthesis, concentration of proline and expression of caspase-3, cleaved caspases -3 and -9, iNOS, NF-κB, COX-2 and AMPKβ. PRODH/POX knock-down contributed to pro-survival autophagy pathways in MCF-7 cells and GlyPro-derived proline augmented this process. However, GlyPro induced apoptosis in PRODH/POX-expressing MCF-7 cells as detected by up-regulation of active caspases -3 and -9. The data suggest that PRODH/POX silencing induces autophagy in MCF-7 cells and GlyPro-derived proline supports this process.

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The effect of adenosine A1 receptor agonist and antagonist on p53 and caspase 3, 8, and 9 expression and apoptosis rate in MCF-7 breast cancer cell line

Cited by 28 publications

References 23 publications

Role of adenosine signaling in the pathogenesis of breast cancer

Role of adenosine signaling in the pathogenesis of breast cancer

Naphthazarin suppresses cell proliferation and induces apoptosis in human colorectal cancer cells via the B-cell lymphoma 2/B-cell associated X protein signaling pathway

Proline oxidase silencing induces proline-dependent pro-survival pathways in MCF-7 cells

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