Progesterone induces apoptosis by activation of caspase-8 and calcitriol via activation of caspase-9 pathways in ovarian and endometrial cancer cells in vitro

McGlorthan, Latoya; Paucarmayta, Ana; Casablanca, Yovanni; Maxwell, G. Larry; Syed, Viqar

doi:10.1007/s10495-021-01657-1

Cited by 37 publications

(29 citation statements)

References 29 publications

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“…The DAPI staining of the cell nuclei indicated apoptotic characteristics such as condensed chromatin, and nuclear fragmentation [ 60 ]. Recently, progesterone (20 µM) was shown to trigger apoptosis via the activation of caspase-8 in ovarian and endometrial cancer cells [ 61 ]. A similar effect was noticed for LNG.…”

Section: Discussionmentioning

confidence: 99%

Insights into the Behavior of Triple-Negative MDA-MB-231 Breast Carcinoma Cells Following the Treatment with 17β-Ethinylestradiol and Levonorgestrel

et al. 2021

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Oral contraceptives (OCs) are widely used due to their efficiency in preventing unplanned pregnancies and treating several human illnesses. Despite their medical value, the toxicity of OCs remains a public concern. Previous studies indicate the carcinogenic potential of synthetic sex hormones and their link to the development and progression of hormone-dependent malignancies such as breast cancer. However, little is known about their influence on the evolution of triple-negative breast carcinoma (TNBC), a malignancy defined by the absence of estrogen, progesterone, and HER2 receptors. This study reveals that the active ingredients of modern OCs, 17β-Ethinylestradiol, Levonorgestrel, and their combination induce differential effects in MDA-MB-231 TNBC cells. The most relevant behavioral changes occurred after the 24 h treatment with 17β-Ethinylestradiol, summarized as follows: (i) decreased cell viability (64.32% at 10 µM); (ii) cell roundness and loss of confluence; (iii) apoptotic aspect of cell nuclei (fragmentation, membrane blebbing); and (iv) inhibited cell migration, suggesting a potential anticancer effect. Conversely, Levonorgestrel was generally associated with a proliferative activity. The association of the two OCs exerted similar effects as 17β-Ethinylestradiol but was less effective. Further studies are necessary to elucidate the hormones’ cytotoxic mechanism of action on TNBC cells.

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Section: Discussionmentioning

confidence: 99%

Insights into the Behavior of Triple-Negative MDA-MB-231 Breast Carcinoma Cells Following the Treatment with 17β-Ethinylestradiol and Levonorgestrel

et al. 2021

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“…In this way, it favors the release of cytochrome C from mitochondria and the activation of caspases 3 and 9 that lead to apoptosis promoted by a variety of signals [ 116 , 117 ]. Moreover, 1,25-(OH) 2 D 3 induces apoptosis in ovarian carcinoma cells by caspase 9 activation [ 164 ] and by downregulation of telomerase reverse transcriptase (hTERT) via the induction of miR-498 [ 165 , 166 ]. Intriguingly, while the aforementioned effects seem to be independent of the TP53 gene, a study has proposed that mutant p53 protein interacts physically with VDR in breast cancer cells, converting the ligand into an anti-apoptotic agent by mechanisms that remain unclear [ 167 ].…”

Section: Mechanisms Introductionmentioning

confidence: 99%

Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms

2022

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This is a narrative review of the evidence supporting vitamin D’s anticancer actions. The first section reviews the findings from ecological studies of cancer with respect to indices of solar radiation, which found a reduced risk of incidence and mortality for approximately 23 types of cancer. Meta-analyses of observational studies reported the inverse correlations of serum 25-hydroxyvitamin D [25(OH)D] with the incidence of 12 types of cancer. Case-control studies with a 25(OH)D concentration measured near the time of cancer diagnosis are stronger than nested case-control and cohort studies as long follow-up times reduce the correlations due to changes in 25(OH)D with time. There is no evidence that undiagnosed cancer reduces 25(OH)D concentrations unless the cancer is at a very advanced stage. Meta-analyses of cancer incidence with respect to dietary intake have had limited success due to the low amount of vitamin D in most diets. An analysis of 25(OH)D-cancer incidence rates suggests that achieving 80 ng/mL vs. 10 ng/mL would reduce cancer incidence rates by 70 ± 10%. Clinical trials have provided limited support for the UVB-vitamin D-cancer hypothesis due to poor design and execution. In recent decades, many experimental studies in cultured cells and animal models have described a wide range of anticancer effects of vitamin D compounds. This paper will review studies showing the inhibition of tumor cell proliferation, dedifferentiation, and invasion together with the sensitization to proapoptotic agents. Moreover, 1,25-(OH)2D3 and other vitamin D receptor agonists modulate the biology of several types of stromal cells such as fibroblasts, endothelial and immune cells in a way that interferes the apparition of metastases. In sum, the available mechanistic data support the global protective action of vitamin D against several important types of cancer.

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“…Through FADD, procaspase‐8 or ‐10 is activated by autocatalysis, leading to the activation of effector caspase (caspase‐3) and the proapoptotic protein Bid. The cleavage form of Bid (tBid) translocates to the mitochondria, which then triggers the intrinsic mitochondrial pathway by altering the MMP (Agrawal, 2019; Fang et al, 2018; McGlorthan et al, 2021; Mühlethaler‐Mottet et al, 2011). According to our experimental results, we could roughly deduce the pathway of the NCB‐induced apoptosis of AW1 cells.…”

Section: Discussionmentioning

confidence: 99%

Neochamaejasmin B extracted from Stellera chamaejasme L. induces apoptosis through caspase‐10‐dependent way in insect neuronal cells

Jiang

et al. 2022

Arch Insect Biochem Physiol

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To explore the toxicity mechanisms of neochamaejasmin B (NCB) extracted from Stellera chamaejasme L., we first evaluated its cytotoxicity in neuronal cells of Helicoverpa zea (AW1 cells). NCB inhibited cell growth and was cytotoxic to AW1 cells in a dose-dependent manner.Further, transmission electron microscopy (TEM) was used to analyze the microstructure, and typical apoptotic characteristics were observed in AW1 cells treated with NCB. Moreover, the NCB-induced apoptosis was dose dependent. Subsequently, we explored the mechanism of apoptosis. A decline in the mitochondrial membrane potential (MMP) was found. Also, the levels of Bax were increased with increases in drug concentration, but there was no statistical difference in Bcl-2 levels at different NCB doses. Caspase-3 and caspase-10 activity was increased.These findings confirmed that NCB induced apoptosis in AW1 cells through a caspase-10-dependent mechanism.The results provide the basic information needed for understanding the toxicity and mechanisms of action of NCB, which could potentially be used to develop NCB as a new insecticide.

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Progesterone induces apoptosis by activation of caspase-8 and calcitriol via activation of caspase-9 pathways in ovarian and endometrial cancer cells in vitro

Cited by 37 publications

References 29 publications

Insights into the Behavior of Triple-Negative MDA-MB-231 Breast Carcinoma Cells Following the Treatment with 17β-Ethinylestradiol and Levonorgestrel

Insights into the Behavior of Triple-Negative MDA-MB-231 Breast Carcinoma Cells Following the Treatment with 17β-Ethinylestradiol and Levonorgestrel

Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms

Neochamaejasmin B extracted from Stellera chamaejasme L. induces apoptosis through caspase‐10‐dependent way in insect neuronal cells

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