A Theoretical Model for the Cell Cycle and Drug Induced Cell Cycle Arrest of FUCCI Systems with Cell-to-Cell Variation during Mitosis

Bae, Hyeonjeong; Go, Young-Hyun; Kwon, Tae-Yong; Sung, Bong June; Cha, Hyuk‐Jin

doi:10.1007/s11095-019-2570-2

Cited by 11 publications

(4 citation statements)

References 34 publications

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“…Previous studies of cell synchronization using FUCCI induce the synchronization using methods including serum starvation, cell cycle-inhibiting drugs, environmental pH or contact inhibition [10][11][12][13][14][15]. Our assays are prepared using a standard method [10] normally thought to produce asynchronous populations, and we take utmost care to ensure that there is no induced synchronization in our cell cultures due to serum starvation, low pH or contact inhibition (electronic supplementary material, S1).…”

Section: Introductionmentioning

confidence: 99%

Mathematical models incorporating a multi-stage cell cycle replicate normally-hidden inherent synchronization in cell proliferation

Vittadello

McCue

Gunasingh

et al. 2019

J. R. Soc. Interface.

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We present a suite of experimental data showing that cell proliferation assays, prepared using standard methods thought to produce asynchronous cell populations, persistently exhibit inherent synchronization. Our experiments use fluorescent cell cycle indicators to reveal the normally hidden cell synchronization, by highlighting oscillatory subpopulations within the total cell population. These oscillatory subpopulations would never be observed without these cell cycle indicators. On the other hand, our experimental data show that the total cell population appears to grow exponentially, as in an asynchronous population. We reconcile these seemingly inconsistent observations by employing a multi-stage mathematical model of cell proliferation that can replicate the oscillatory subpopulations. Our study has important implications for understanding and improving experimental reproducibility. In particular, inherent synchronization may affect the experimental reproducibility of studies aiming to investigate cell cycle-dependent mechanisms, including changes in migration and drug response.

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Section: Introductionmentioning

confidence: 99%

Mathematical models incorporating a multi-stage cell cycle replicate normally-hidden inherent synchronization in cell proliferation

Vittadello

McCue

Gunasingh

et al. 2019

J. R. Soc. Interface.

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“…The morphological and cell cycle quantitative assessments in this study further suggested that INT 747 treatment-induced cell death and eventually cell cycle arrest. The cell cycle is the basis for cell proliferation (31) . Our results further show that INT 747 increases the fraction of cells in the G1 phase of the PC-3 cells, illuminating that some cells are blocked at the G1 phase.…”

Section: Discussionmentioning

confidence: 99%

Role of Fasting Mimicking Diet in Farnesoid x Receptor for Suppressing Epithelial-to-Mesenchymal Transition, Cell Cycle Progression, and Viability of Prostate Cancer Cells

Wrood Salim,

Sameh Arif,

Talib Al-sudani

2023

IJPS

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The systemic and resistant nature of metastatic castration-resistant prostate cancers (mCRPC) renders it largely incurable even after intensive multimodal therapy. Proliferation, survival, and epithelial-mesenchymal transition (EMT) are three fundamental events that are deeply linked to carcinogenesis. Hence, it is necessary to find a new combination of several therapies, targeting those vital mechanisms without causing side effects. Significant research works have shown differential low expression of the metabolic Farnesoid X receptor (FXR) in primary and metastatic prostate cancer suggesting their importance in prostate pathogenesis. Obticholic acid (INT 747), a potent FXR agonist is widely used in primary biliary cholangitis, and Fasting mimicking Diet (FMD) both were drastically showed effects on different cancer progression. We hypothesized that FXR and FMD may inhibit proliferation and the metastatic phenotype in PC-3 prostate cancer cells. Analyses of the cell viability, cell cycle, migration, and matrigel invasion assays were performed to elucidate how INT 747 and /or FMD functions in prostate cancer. In this study, INT 747 treatment caused apoptotic morphological changes and significantly reduced the survival of PC-3 cells incubated in normal mediums. Furthermore, we showed that the combination of the INT 747 and FMD was much more harmful to cancer cells than the treatment with INT 747 or FMD alone. Moreover, our study showed that INT 747 either alone or combined with FMD robustly induced cell cycle arrest at the S phase. Interestingly, the combination treatment on PC-3 cells not only showed several lines of evidence of apoptotic cells death but also inhibited carcinogenic potential as evaluated by impairment of spheroid formation capacity and delayed wound healing and matrigel invasion. At the cellular level, FXR activation resulted in down-regulation of procaspase -3, vimentin, and MMP9, which triggers apoptotic cell death, cell cycle arrest, and switch from mesenchymal to an epithelial phenotype. Collectively, FXR activation alone markedly decreases, and when combined with FMD abrogates the survival and carcinogenic potential of metastatic prostate cancer cells.

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“…Mitosis and cytokinesis are defined as the cleavage phase of the cell cycle, or the M phase. This process produces two daughter cells that are identical to the parent cell gene [15][16][17] . This process typically accounts for about 10% of the entire cell cycle.…”

Section: Discussionmentioning

confidence: 99%

Abound Hepatic Mitosis: Unusual Morphology in the Intrahepatic Cholelithiasis Patient

Wang

Jiang

Wang

et al. 2021

Jour. of oncol. res.

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To explore the clinicopathological features of abound mitosis of the hepatocytes in intrahepatic cholelithiasis. The clinicopathological data of one case diagnosed as intrahepatic cholelithiasis was collected from Yantai Yuhuangding Hospital and the clinicopathological characters were discussed. A 68-year-old man suffered from the pain in the right upper quadrant and radiology showed multiple stones in the gallbladder and left liver. The images suggested intrahepatic cholelithiasis. The patient received gallbladder and partial hepatectomy. A large number of mitosis was observed and twelve nuclear fissions were found under high magnification, even in some area pathological nuclear fission could be observed in morphology. On the basis of detection in laboratory, the diagnosis of intrahepatic cholelithiasis was made. The patient did not receive any therapy after surgery. The patient was in a good condition after 18 months follow-up. Increased number of hepatic mitosis might be due to the stimulation from stones, hepatic biliary or secondary inflammatory. High index of proliferation should be prevented from the potential misdiagnosis of hepatic tumor.

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A Theoretical Model for the Cell Cycle and Drug Induced Cell Cycle Arrest of FUCCI Systems with Cell-to-Cell Variation during Mitosis

Cited by 11 publications

References 34 publications

Mathematical models incorporating a multi-stage cell cycle replicate normally-hidden inherent synchronization in cell proliferation

Mathematical models incorporating a multi-stage cell cycle replicate normally-hidden inherent synchronization in cell proliferation

Role of Fasting Mimicking Diet in Farnesoid x Receptor for Suppressing Epithelial-to-Mesenchymal Transition, Cell Cycle Progression, and Viability of Prostate Cancer Cells

Abound Hepatic Mitosis: Unusual Morphology in the Intrahepatic Cholelithiasis Patient

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