5-Fluorouracil attenuates an oncostatic effect of melatonin on estrogen-sensitive human breast cancer cells (MCF7)

Furuya, Yoshihiko; Yamamoto, Kei; Kohno, Norio; Ku, Yonsun; Saitoh, Y

doi:10.1016/0304-3835(94)90170-8

Cited by 18 publications

(7 citation statements)

References 4 publications

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“…Melatonin was administered to different cell lines and found to have oncostatic effects. Reports suggest that melatonin treatment reduced cell growth in MCF7 (human breast carcinoma cell line) (Liburdy et al, 1993;Furuya et al, 1994;Cos et al, 1996Cos et al, , 2002Leon-Blanco et al, 2003;Cucina et al, 2009;Martinez-Campa et al, 2009;Chottanapund et al, 2014), BG1 (ovarian carcinoma cell line) (Petranka The cell cycle analysis of the 5RP7 cells was read by flow cytometry. The melatonin provided the arrest of the 5RP7 cells in the G1 phase.…”

Section: Discussionmentioning

confidence: 99%

Melatonin induces antiproliferative activity through modulation of apoptoticpathway in H-ras oncogene transformed 5RP7 cells

Kaplan

Çiftçi²,

Kutlu³

2015

Turk J Biol

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IntroductionOncogenes are important factors in the carcinogenesis process. Cancer cells may demonstrate an uncontrolled proliferation due to oncogenes. Ras is one of these oncogenes, and it is responsible for cell differentiation/ proliferation. It is well known that ras mutation occurs in human tumors such as pancreatic, thyroid, and colon cancers. H-ras, K-ras, and N-ras proteins belonging to the ras family play a role in cancer diseases (Brunner et al., 2004). Thus, ras genes are effective targets for anticancer drug development (Weiwer et al., 2012). In this study, we used H-ras oncogene transformed 5RP7 cells. These cells were obtained from embryonic tissues of Rattus norvegicus and transformed by the H-ras oncogene.Melatonin (N-acetyl-5-methoxytryptamine) is a methoxyindole secretory product as a natural compound, which is produced by the pineal gland and a variety of organs (such as the retina, Harderian glands, gut, ovary, testes, or bone marrow) during the dark phase (Leon-

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Section: Discussionmentioning

confidence: 99%

Melatonin induces antiproliferative activity through modulation of apoptoticpathway in H-ras oncogene transformed 5RP7 cells

Kaplan

Çiftçi²,

Kutlu³

2015

Turk J Biol

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“…Melatonin has been widely shown to inhibit the growth of several types of cancer cells, including breast cancer cells [Liburdy et al, 1993;Furuya et al, 1994;Cos and Sanchez-Barcelo, 1995;Lemus-Wilson et al, 1995], human cervical cancer cells [Chen et al, 1995], lymphoid cells [Persengiev and Kyurkchiev, 1993], melanoma cells [Slominski and Pruski, 1993;Ying et al, 1993], neuroblastoma cells [Cos et al, 1996], and ovarian carcinoma cells [Petranka et al, 1999]. Treatment of cancer cells with melatonin results in an alteration of cell cycle kinetics.…”

Section: Discussionmentioning

confidence: 99%

Effect of melatonin on cell growth, metabolic activity, and cell cycle distribution

Natarajan¹,

Reíter

Meltz³

et al. 2001

Journal of Pineal Research

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We have recently demonstrated that the pineal secretory product melatonin inhibits the key transcriptional regulator nuclear factor-kappa B (NF-kappa B). As the activation of NF-kappa B is known to regulate the expression of cellular genes associated with cell cycle progression, cell growth, and differentiation, we investigated the effect of melatonin treatment on several cellular processes. These include cell viability, metabolic activity, and cell cycle phase distribution. Human embryonic kidney (293S) cells were treated with melatonin at concentrations of 0.02, 0.2, or 2 mM. When cell viability was measured 24, 48, and 72 hr after continuous exposure to melatonin using the trypan blue dye exclusion method, no significant cell death was observed. Even after exposure to 2 mM melatonin for 72 hr, cell viability remained at 98%. In contrast, another antioxidant compound, pyrrolidine dithiocarbomate (PDTC), at a 2 mM concentration reduced cell viability to 80.7+/-2.1% as early as 24 hr compared with untreated controls (P<0.05). When the metabolic activity was determined at 24, 48, and 72 hr using the colorimetric MTT assay, no significant changes in metabolic activity were observed. Even if the cells were treated with 10 mM melatonin for 72 hr, the metabolic activity was similar to that of the control cells. When cell cycle analysis was performed by flow cytometry, no marked difference in cell cycle distribution was observed. Melatonin at a concentration of 2 mM, however, did slightly alter the cell cycle (percentage of S phase cells) at 48 hr. This study revealed that when 293S cells are treated with concentrations of melatonin up to 2 mM, no significant alterations in three important cellular functions occurred. Exogenously added melatonin appeared to have a limited influence on the normal functioning of the cells even when the exposure continued for 72 hr.

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“…While the concentration of E2 might be low, its effect might not be negligible because a direct mitogenic effect of exogenous E2 on MCF7 can be initiated as low as 3 pM and maximized at 0.2 to 10nM. 100 Furthermore, other than estrogen receptors, there exist nonspecific bindings between estrogen and other elements inside the cell. 101 Therefore, MCF7 cells growing in an E2 condition have a much higher internal concentration of E2 than that of medium due to non-specific binding of E2 in the cytoplasm as well as specific binding of E2 to various estrogen receptors in the cell.…”

Section: Methodsmentioning

confidence: 99%

Modeling breast cancer proliferation, drug synergies, and alternating therapies

He¹,

Demas²,

Shajahan-Haq³

et al. 2023

iScience

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5-Fluorouracil attenuates an oncostatic effect of melatonin on estrogen-sensitive human breast cancer cells (MCF7)

Cited by 18 publications

References 4 publications

Melatonin induces antiproliferative activity through modulation of apoptoticpathway in H-ras oncogene transformed 5RP7 cells

Melatonin induces antiproliferative activity through modulation of apoptoticpathway in H-ras oncogene transformed 5RP7 cells

Effect of melatonin on cell growth, metabolic activity, and cell cycle distribution

Modeling breast cancer proliferation, drug synergies, and alternating therapies

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