Estrogen and Progesterone Lower Cyclin B1 and D1 Expression, Block Cell Cycle in G2/M, and Trigger Apoptosis in Human Adrenal Carcinoma Cell Cultures

Brown, John W.; Prieto, L. M.; Perez‐Stable, Carlos; Montoya, Marı́a E.; Cappell, Steven D.; Fishman, Lawrence M.

doi:10.1055/s-2008-1073140

Cited by 12 publications

(9 citation statements)

References 12 publications

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“…There was no effect of any of these estrogenic compounds on the percentage of cells in S phase in this system. Extension of these studies is needed to understand more fully the growth-inhibitory and apoptotic effects of estrogen on SW-13 human adrenal cortical carcinoma cells in culture shown here and also reported by us elsewhere [11] .…”

Section: Discussionmentioning

confidence: 54%

High Dose 17 β-Estradiol and the α-Estrogen Agonist PPT Trigger Apoptosis in Human Adrenal Carcinoma Cells but the β-Estrogen Agonist DPN Does Not

Prieto¹,

Brown

Perez‐Stable³

et al. 2008

Horm Metab Res

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Previous studies have shown that high dose 17beta-estradiol (10 (-5) M) has a G2/M blocking effect in SW-13 human adrenal carcinoma cultures and strongly enhances apoptosis. To examine the differential effects of estrogen alpha and beta-receptors in this system, we incubated SW-13 cells with specific alpha- and beta-estrogen receptor agonists, PPT [4,4',4''-(propyl-[ (1)H]-pyrazole-1,3,5-triyl) trisphenol] and DPN [2,3-bis (4-hydroxyphenyl) propionitrile], respectively (each at 10 (-5) M). Flow cytometry was used to analyze the percentages of cells in various phases of the cell cycle [sub-G1 (apoptosis), G1, S, and G2/M] in each experimental condition. Exposure to 17 beta-estradiol for 48 hours increased apoptosis more than 5-fold (from 3.6+/-0.5 to 20+/-2.2% of cells; p<0.01). The alpha-estrogen agonist PPT had a similar effect, increasing apoptosis to 22+/-1.7% (p<0.01), but the beta-agonist DPN caused no change (3.6+/-0.5 vs. 3.9+/-0.8%). While estrogen and the alpha-estrogen agonist decrease apoptosis in this system, both of these compounds decreased the percentage of cells in G1 (from 59+/-1.4% for control to 34+/-2.3% for estrogen and 40+/-2.0% for PPT; p<0.01 for both agents relative to control); the beta-agonist again had no effect. Estrogen was also found to block the cell cycle in G2/M, increasing it from 15+/-0.4 to 21+/-1.0% of cells (p<0.01), but neither the alpha- nor beta-estrogen agonists had any effect at this point in the cell cycle, indicating that the influence of estrogen was not likely to be either alpha- or beta-receptor mediated. There was no apparent effect of any of these agents on DNA synthesis, as indicated by unchanged percentages of cells in S phase. These studies suggest that induction of apoptosis by estrogen in SW-13 human adrenal cortical carcinoma cultures is mediated by the alpha-receptor, but the G2/M blocking effect of estrogen is not likely to be related to either alpha or beta mechanisms.

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Section: Discussionmentioning

confidence: 54%

High Dose 17 β-Estradiol and the α-Estrogen Agonist PPT Trigger Apoptosis in Human Adrenal Carcinoma Cells but the β-Estrogen Agonist DPN Does Not

Prieto¹,

Brown

Perez‐Stable³

et al. 2008

Horm Metab Res

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“…The control of G2/M phase transition involves two critical molecules, cyclin B1 and CDK1, the down-regulation of which has been demonstrated to result in the delay of M phase entry[54][55][56][57]. Furthermore, it…”

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confidence: 99%

Mechanisms of tolvaptan-induced toxicity in HepG2 cells

Beland

Chen

et al. 2015

Biochemical Pharmacology

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Tolvaptan, a vasopressin receptor 2 antagonist used to treat hyponatremia, has recently been reported to be associated with an increased risk of liver injury. In this study, we explored the underlying mechanisms of hepatotoxicity of tolvaptan using human HepG2 cells. Tolvaptan inhibited cell growth and caused cell death in a concentration- and time-dependent manner. Tolvaptan treatment led to delayed cell cycle progression, accompanied by decreased levels of several cyclins and cyclin-dependent kinases. Tolvaptan was found to cause DNA damage, as assessed by alkaline comet assays; this was confirmed by increased levels of 8-oxoguanine and phosphorylation of histone H2AX. Exposure of HepG2 cells to tolvaptan enhanced cytochrome C release and triggered apoptosis by modulating Bcl-2 family members. The activation of p38 contributed to tolvaptan-mediated apoptosis via down-regulation of Bcl-2. Proteasome inhibition altered tolvaptan-induced cell cycle deregulation and enhanced tolvaptan-induced apoptosis and cytotoxicity. Moreover, tolvaptan treatment induced autophagy. Inhibition of autophagy by knocking-down an autophagy-related gene increased tolvaptan-induced apoptosis and cytotoxicity. Taken together, our findings suggest that the cytotoxicity of tolvaptan results from delayed cell cycle progression, the induction of DNA damage, and the execution of apoptosis. In addition, a number of signaling pathways were perturbed by tolvaptan and played an important role in its cytotoxicity.

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“…For examples, maple polyphenols, ginnalins A-C, can arrest the MCF7 breast cancer cells in the G2/M phase and decrease the Cyclin D1 protein level 49 . Additionally, 17 β-estradiol and progesterone induce the G2/M arrest and the reduction of cyclin B1 and D1 in SW-13 human adrenal carcinoma cells 50 . The mechanism by which the reduction of CyclinD1 expression contributes to the cell cycle G2/M arrest in SW527 is unknown at present.…”

Section: Discussionmentioning

confidence: 94%

KHF16 is a Leading Structure from Cimicifuga foetida that Suppresses Breast Cancer Partially by Inhibiting the NF-κB Signaling Pathway

Kong¹,

Li²,

Nian³

et al. 2016

Theranostics

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Triterpenoids extracted from Cimicifuga foetida have been reported to inhibit cancer by inducing cell cycle arrest and apoptosis. In this study, KHF16 (24-acetylisodahurinol-3-O-β-D-xylopyranoside), a cycloartane triterpenoid isolated from the rhizomes of C. foetida, showed potent anti-cancer activity in multiple ERα/PR/HER2 triple-negative breast cancer (TNBC) cell lines. KHF16 significantly induces cell cycle G2/M phase arrest and apoptosis in both MDA-MB-468 and SW527 TNBC cell lines. KHF16 reduces the expression levels of XIAP, Mcl-1, Survivin and Cyclin B1/D1 proteins. Importantly, KHF16 inhibits TNFα-induced IKKα/β phosphorylation, IKBα phosphorylation, p65 nuclear translocation and NF-κB downstream target gene expression, including XIAP, Mcl-1 and Survivin, in TNBC cells. These results suggest that KHF16 may inhibit TNBC by blocking the NF-κB signaling pathway in part.

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Estrogen and Progesterone Lower Cyclin B1 and D1 Expression, Block Cell Cycle in G2/M, and Trigger Apoptosis in Human Adrenal Carcinoma Cell Cultures

Cited by 12 publications

References 12 publications

High Dose 17 β-Estradiol and the α-Estrogen Agonist PPT Trigger Apoptosis in Human Adrenal Carcinoma Cells but the β-Estrogen Agonist DPN Does Not

High Dose 17 β-Estradiol and the α-Estrogen Agonist PPT Trigger Apoptosis in Human Adrenal Carcinoma Cells but the β-Estrogen Agonist DPN Does Not

Mechanisms of tolvaptan-induced toxicity in HepG2 cells

KHF16 is a Leading Structure from Cimicifuga foetida that Suppresses Breast Cancer Partially by Inhibiting the NF-κB Signaling Pathway

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