Cell Cycle: Regulation by Cyclins

Truman, Andrew W.; Kitazono, Ana A.; Gerald, Jonathan N. Fitz; Kron, Stephen J.

doi:10.1002/9780470015902.a0001364.pub3

Cited by 3 publications

(3 citation statements)

References 38 publications

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“…This difference holds true and is clear in chimeras where both species-specific states can be observed in the same sample. Given the strong conservation of cyclins among highly disparate taxa (Swenson et al, 1986; Truman et al, 2001), we were surprised by such differences in cyclin regulation within birds. Our data support the possibility that differences in the expression or post-translational processing of even one cell cycle regulator may greatly impact species-specific adaptive evolution.…”

Section: Discussionmentioning

confidence: 99%

Evolution of a developmental mechanism: Species-specific regulation of the cell cycle and the timing of events during craniofacial osteogenesis

Hall

Jheon

Ealba

et al. 2014

Developmental Biology

109

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Neural crest mesenchyme (NCM) controls species-specific pattern in the craniofacial skeleton but how this cell population accomplishes such a complex task remains unclear. To elucidate mechanisms through which NCM directs skeletal development and evolution, we made chimeras from quail and duck embryos, which differ markedly in their craniofacial morphology and maturation rates. We show that quail NCM, when transplanted into duck, maintains its faster timetable for development and autonomously executes molecular and cellular programs for the induction, differentiation, and mineralization of bone, including premature expression of osteogenic genes such as Runx2 and Col1a1. In contrast, the duck host systemic environment appears to be relatively permissive and supports osteogenesis independently by providing circulating minerals and a vascular network. Further experiments reveal that NCM establishes the timing of osteogenesis by regulating cell cycle progression in a stage- and species-specific manner. Altering the time-course of D-type cyclin expression mimics chimeras by accelerating expression of Runx2 and Col1a1. We also discover higher endogenous expression of Runx2 in quail coincident with their smaller craniofacial skeletons, and by prematurely over-expressing Runx2 in chick embryos we reduce the overall size of the craniofacial skeleton. Thus, our work suggests that NCM establishes species-specific size in the craniofacial skeleton by controlling cell cycle, Runx2 expression, and the timing of key events during osteogenesis.

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Section: Discussionmentioning

confidence: 99%

Evolution of a developmental mechanism: Species-specific regulation of the cell cycle and the timing of events during craniofacial osteogenesis

Hall

Jheon

Ealba

et al. 2014

Developmental Biology

109

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“…We saw consistent decreases in protein levels of cyclins A2, B1 and D1. We also noted consistent and marked decreases in CDK2 and CDK4 protein levels, which was regulated by the interplay of cyclins and CDK inhibitors (King, Deshaies et al 1996, Cayrol and Ducommun 1998, Ekholm and Reed 2000, Truman, Kitazono et al 2001, Amanatullah, Zafonte et al 2002. Surprisingly, R5020 treatment caused a remarkable increase of cyclin E1.…”

Section: R5020 Altered the Expression Of Cyclins And Cdks In Mcf-7-prsupporting

confidence: 64%

“…Cyclin-dependent kinases (CDKs) are also essential proteins involved in the regulation of cell cycle. During the cell cycle, expression of CDKs remains constant and CDK kinase activity is regulated by interaction with two groups of proteins: cyclins and CDK inhibitors (Ekholm and Reed 2000, Miller and Cross 2001, Truman, Kitazono et al 2001). R5020's effect on cyclins and…”

Section: Cdksmentioning

confidence: 99%

Defining the role of progesterone receptor and progestin in luminal breast cancer cells

Bajalovic¹

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Progesterone is a steroid hormone essential for the reproduction and the development of the mammary gland. Its effects are mediated by progesterone receptor (PR) which is induced by estrogen in most target tissues. In humans and mice, PR is expressed as two major isoforms: PRA and PRB. Although progesterone has been implicated in breast cancer its role in the development of breast cancer remains controversial. There is evidence for the increased risk of breast cancer incidence in post-menopausal women receiving estrogen plus progestin replacement therapy compared to estrogen therapy alone. However, progestin demonstrated therapeutic benefits for metastatic breast cancer. In laboratory studies, progestin can stimulate or inhibit cell growth depending on experimental conditions and cell models. It has been reported that progesterone inhibits estrogen-induced growth of ER and PR-positive luminal breast cancer cells MCF-7 in xenograft model and this is mediated by modulating the activity of ER. However, the role of PR in mediating the effect of progestin in this most commonly used ER and PR-positive model is controversial. This is partly due to the fact that PR expression is estrogen-dependent and the level of estrogen-induced PR is relatively low. As a result, the effect of progestin treatment is often marginal. In order to better understand PRmediated effect of progestin in luminal breast cancer, the main aim of the study was to establish MCF-7 luminal breast cancer cells overexpressing PRB and define the molecular and cellular aspects of PRB-mediated effect of progestin in this MCF-7 cell model. We hypothesize that progestin exerts inhibitory effect on MCF-7 cells expressing PR independent estrogen. The study demonstrated that progestin R5020 causes drastic cell growth inhibition. More interestingly, R5020 completely abolished estrogen-induced cell growth. Furthermore, the R5020-treated cells in three dimensional (3D) Matrigel culture were unable to form proper mammospheres and almost the entire population underwent apoptosis after 1-2 weeks in 3D culture. Thus, progestin R5020 strongly suppresses the growth of luminal breast cancer cells when there is abundant expression of PRB. Taken together, our study demonstrated powerful anti-tumoral effect of R5020 on breast cancer cells expressing high levels of PR a nd future in vivo studies could lead to improved outcomes in breast cancer patients. Chapter 1. Introduction 1.1 Nuclear receptors Nuclear receptors (NRs) are part of a large family of ligand-activated transcription factors (Tsai and O'Malley 1994, Glass and Rosenfeld 2000). Based on their different mechanisms of action and ligand properties, NRs superfamily can be classified into three groups (hormone, metabolic and orphan NRs) (Mangelsdorf, Thummel et al. 1995). These transcription factors directly regulate genes that are involved in numerous physiological processes, such as homeostasis, reproduction, development, and metabolism (Mangelsdorf, Thummel et al. 1995, Xiao, Wang et al. 2013). NRs exert their func...

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Öncül Afidikolin ve Nokodazol Muamelesinin Kanserli ve Ölümsüzleştirilmiş Mezotelyum Hücrelerinde Kapsaisin Sitotoksitesine Etkisi

Cömertpay

Ceylan

2019

Kahramanmaraş Sütçü İmam Üniversitesi Tarım Ve Doğa Dergisi

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ÖZET Malignant mezoteliyoma akciğer, kalp ve karın zarında gelişen bir kanser türüdür. Kapsaisin, Capsicum spp.cinsi bitkilerde üretilen ikincil bir metabolittir ve bazı kanser hücreleri üzerinde sitotoksik etkisi olduğu gösterilmiştir. Afidokolin ve nokadozol, hücreleri sırasıyla G1/S ve G2/M fazında tutar. Bu çalışmada, kanserli (H2452) ve ölümsüzleştirilmiş (AG07086) mezotelyum hücrelerinin kapsaisin sitotoksisitesi, afidokolin ve nokodazol ön muamelesi ile, ya da bu muameleler olmaksızın, MTS tekniğiyle belirlenmiş ve kaspaz-3 mRNA seviyesindeki değişiklikler qRT-PCR metoduyla incelenmiştir. Elde edilen bulgulara göre; i) normal koşullarda, kanserli ve ölümsüzleştirilmiş mezotelyum hücrelerinde kapsaisin sitotokisitesi benzerdir (p>0.05), ii) afidikolin muamelesiyle kapsaisinin etkenliği azalmış (p<0.05) ancak kanser hücrelerinin kapsaisin duyarlılığı ölümsüz hücrelere kıyasla yükselmiştir (p<0.05), iii) nokodazol ön muamelesi ile, kanser hücrelerinde kapsaisinin sitotoksik etkisi düşüş göstermiş (p<0.05), ancak ölümsüzleştirilmiş hücreler için bu değişim istatiksel olarak anlamsız bulunmuştur (p>0.05), iv) yapılan tüm uygulamalarda kaspaz-3 mRNA miktarı kontrol grubuna denk çıkmıştır (p>0.05). ABSTRACTMalignant mesothelioma is a type of cancer, developing from the lung membrane, heart and stomach. Capsaicin is a secondary metabolite produced in Capsicum spp., which has been demonstrated to have cytotoxic effect on various cancer types. Aphidicolin and nocadozole are known to arrest cells in G1/S and G2/M, respectively. In this study, the cytotoxicity of capsaicin on cancerous (H2452) and immortalized (AG07086) cells of mesothelium, with or without primary exposure to aphidicolin or nocadozole, was determined through MTS method and the fluctuations in caspase-3 mRNA levels were investigated by qRT-PCR. Accordingly i) under regular conditions, capsaicin cytotoxicity on cancerous and immortalized cells of mesothelium was similar (p>0.05), ii) aphidicolin pre-exposure decreased the cytotoxicity of capsaicin on cancerous cells (p<0.05), yet it increased their sensitivity to capsaicin (p<0.05), iii) pre-exposure to nocodazole decreased the cytotoxicity on cancerous cells (p<0.05) whereas it did not affect it for the immortalized cells (p>0.05), iv) in all conditions studied, caspase-3 mRNA levels were analogous to the control (p>0.05).

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Cell Cycle: Regulation by Cyclins

Cited by 3 publications

References 38 publications

Evolution of a developmental mechanism: Species-specific regulation of the cell cycle and the timing of events during craniofacial osteogenesis

Evolution of a developmental mechanism: Species-specific regulation of the cell cycle and the timing of events during craniofacial osteogenesis

Defining the role of progesterone receptor and progestin in luminal breast cancer cells

Öncül Afidikolin ve Nokodazol Muamelesinin Kanserli ve Ölümsüzleştirilmiş Mezotelyum Hücrelerinde Kapsaisin Sitotoksitesine Etkisi

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