Additive Inhibition of RL95-2 Endometrial Carcinoma Cell Growth by Carboplatin and 1,25 Dihydroxyvitamin D3

Saunders, Dwight E.; Christensen, Carl W.; Wappler, N.L.; Cho, Y.L.; Lawrence, W. Dwayne; Malone, John M.; Malviya, Vinay K.; Deppe, Gunter

doi:10.1006/gyno.1993.1264

Cited by 8 publications

(4 citation statements)

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“…Saunders et al (22) found additive inhibition of endometrial carcinoma cell growth by carboplatin and calcitriol. Lee et al (17) studied anti-tumor effects of progesterone and 1,25-D3 in endometrial cancer cell lines and immortalized human The VDR was detected in 14 of the 21 specimens.…”

Section: Discussionmentioning

confidence: 99%

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Paclitaxel, Carboplatin and 1,25-D3 Inhibit Proliferation of Endometrial Cancer Cells In Vitro

Kuittinen

Rovio

Staff

et al. 2017

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Abstract. Background/Aim: Endometrial cancer cells areknown to be sensitive to carboplatin and paclitaxel. Furthermore, vitamin D (1, Endometrial cancer is the most common gynecological malignancy in developed countries. In Finland incidence is 13.9 per 100,000 persons a year (1). Most women are diagnosed with early-stage disease and have a high cure rate with surgery alone with a reported 5-year survival rate of 90% (2). Still up to 25% of women will have advanced, high grade or recurrent disease and require additional treatment. In these cases, the therapeutic response to cytotoxic and hormonal agents has been typically only partial and of short duration. There is no generally accepted standard chemotherapy in treatment of advanced and recurrent endometrial carcinoma but simultaneous administration of carboplatin and paclitaxel or carboplatin and pegylated liposomal doxorubicin are widely used (3-8).Vitamin D is an antiproliferative and immunomodulatory secosteroid hormone with a well-established role in maintenance of calcium synthesis. Active metabolite of vitamin D, 1alpha,25-dihydroxyvitamin D 3 (1,25-D3) binds to the vitamin D receptor (VDR) in the cell nucleus. The function and/or expression of the VDR is needed for the 6575 This Αrticle is freely accessible online.Correspondence to:

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Section: Discussionmentioning

confidence: 99%

“…1,25-D3 is a potential antitumor agent because of its ability to regulate cancer cell growth. 1,25-D3 has been found to inhibit endometrial cancer cell growth both as a single agent (21) and combined with carboplatin (22).…”

mentioning

confidence: 99%

Paclitaxel, Carboplatin and 1,25-D3 Inhibit Proliferation of Endometrial Cancer Cells In Vitro

Kuittinen

Rovio

Staff

et al. 2017

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“…Saunders and colleagues highlighted the inhibitory effect of VD treatment on the growth of endometrial carcinoma cells (RL95-2) for the first time. Unfortunately, these authors did not investigate the presence of VDR and the molecular mechanism to account for the observation [57]. Later, Yabushita and colleagues (1996) demonstrated that the growth of RL95-2 cells expressing VDR was prevented in a dose-dependent manner by VD treatment (inhibited to 44% following treatment with 50 nM of 1,25(OH) 2 D 3 for 6 days); on the contrary, the growth of AMEC-1 cells not expressing VDR was completely uninhibited by the treatment [52].…”

Section: Vitamin D and Endometrial Cancermentioning

confidence: 99%

Vitamin D and Endometrium: A Systematic Review of a Neglected Area of Research

Cermisoni

Alteri

Corti

et al. 2018

IJMS

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Growing evidence supports a role of vitamin D (VD) in reproductive health. Vitamin D receptor (VDR) is expressed in the ovary, endometrium, and myometrium. The biological actions of VD in fertility and reproductive tissues have been investigated but mainly using animal models. Conversely, the molecular data addressing the mechanisms underlying VD action in the physiologic endometrium and in endometrial pathologies are still scant. Levels of VDR expression according to the menstrual cycle are yet to be definitively clarified, possibly being lower in the proliferative compared to the secretory phase and in mid-secretory compared to early secretory phase. Endometrial tissue also expresses the enzymes involved in the metabolism of VD. The potential anti-proliferative and anti-inflammatory effects of VD for the treatment of endometriosis have been investigated in recent years. Treatment of ectopic endometrial cells with 1,25(OH)2D3 could significantly reduce cytokine-mediated inflammatory responses. An alteration of VD metabolism in terms of increased 24-hydroxylase mRNA and protein expression has been demonstrated in endometrial cancer, albeit not consistently. The effect of the active form of the vitamin as an anti-proliferative, pro-apoptotic, anti-inflammatory, and differentiation-inducing agent has been demonstrated in various endometrial cancer cell lines.

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“…1,25-(OH)2D3 was shown to potentiate the anti proliferative action of platinum chemotherapeutic drugs in non-prostatic tumor models (Cho et al 1991, Saunders et al 1993. This finding prompted similar studies in prostate cancer cell lines which demonstrated that the combination of 1,25-(OHhD3 or the analog Ro 25-6760 and cis-or carbo platin acts synergistically to decrease prostate cancer cell growth (Moffat et al 1999).…”

Section: Chemotherapeutic and Other Agentsmentioning

confidence: 99%

Steroid Hormones and Cell Cycle Regulation

2002

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Additive Inhibition of RL95-2 Endometrial Carcinoma Cell Growth by Carboplatin and 1,25 Dihydroxyvitamin D3

Cited by 8 publications

References 0 publications

Paclitaxel, Carboplatin and 1,25-D3 Inhibit Proliferation of Endometrial Cancer Cells In Vitro

Paclitaxel, Carboplatin and 1,25-D3 Inhibit Proliferation of Endometrial Cancer Cells In Vitro

Vitamin D and Endometrium: A Systematic Review of a Neglected Area of Research

Steroid Hormones and Cell Cycle Regulation

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