scholarly journals Impact of Variability in Cell Cycle Periodicity on Cell Population Dynamics

2021 ◽  
Author(s):  
Chance Michael Nowak ◽  
Tyler Quarton ◽  
Leonidas Bleris
Keyword(s):  
Cell Cycle ◽  
Population Dynamics ◽  
Cell Population ◽  
Cell Cycle Progression ◽  
Similarity Function ◽  
Cycle Progression ◽  
Cell Population Dynamics ◽  
Model Simulations ◽  
Cell Cycle Synchronization ◽  
Cervical Cancer Cells

Cell cycle synchronization has been pivotal in the development of our understanding of cell population dynamics. Intriguingly, when cells are released from a synchronized state, they do not maintain synchronized cell division and rapidly become asynchronous. Here, using a combination of experiments and model simulations, we investigate this process of "cell cycle desynchronization" in cervical cancer cells (HeLa) that are arrested at the G1/S boundary. We tracked DNA content overtime at regular intervals to monitor cell cycle progression and developed a custom auto-similarity function to quantify the convergence to asynchronicity. In parallel, using experimental data, we developed a single-cell phenomenological model that returns DNA concentration across the cell cycle stages from a desynchronizing cell population. Our simulations revealed that desynchronization is primarily sensitive to cell cycle variability. We tested this prediction by introducing lipopolysaccharide to increase cellular noise, which resulted in greater cell cycle variability with an enhanced rate of desynchronization. Our results show that the desynchronization rate of cell populations can be used a proxy of the degree of variance in cell cycle periodicity.

scholarly journals Oncogenic role of ALX3 in cervical cancer cells through KDM2B-mediated histone demethylation of CDC25A

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jinhong Qi ◽  
Li Zhou ◽  
Dongqing Li ◽  
Jingyuan Yang ◽  
He Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Cervical Squamous Cell Carcinoma ◽  
Cycle Progression ◽  
Normal Tissues ◽  
Positive Regulator ◽  
Cervical Cancer Cells

Abstract Background Cell division cycle 25A (CDC25A) is a well-recognized regulator of cell cycle progression and is involved in cancer development. This work focused on the function of CDC25A in cervical cancer cell growth and the molecules involved. Methods A GEO dataset GSE63514 comprising data of cervical squamous cell carcinoma (CSCC) tissues was used to screen the aberrantly expressed genes in cervical cancer. The CDC25A expression in cancer and normal tissues was predicted in the GEPIA database and that in CSCC and normal cells was determined by RT-qPCR and western blot assays. Downregulation of CDC25A was introduced in CSCC cells to explore its function in cell growth and the cell cycle progression. The potential regulators of CDC25A activity and the possible involved signaling were explored. Results CDC25A was predicted to be overexpressed in CSCC, and high expression of CDC25A was observed in CSCC cells. Downregulation of CDC25A in ME180 and C33A cells reduced cell proliferation and blocked cell cycle progression, and it increased cell apoptosis. ALX3 was a positive regulator of CDC25A through transcription promotion. It recruited a histone demethylase, lysine demethylase 2B (KDM2B), to the CDC25A promoter, which enhanced CDC25A expression through demethylation of H3k4me3. Overexpression of ALX3 in cells blocked the inhibitory effects of CDC25A silencing. CDC25A was found as a positive regulator of the PI3K/Akt signaling pathway. Conclusion This study suggested that the ALX3 increased CDC25A expression through KDM2B-mediated demethylation of H3K4me3, which induced proliferation and cell cycle progression of cervical cancer cells.

Carvacrol Exhibits Chemopreventive Potential against Cervical Cancer Cells via Caspase-Dependent Apoptosis and Abrogation of Cell Cycle Progression

2020 ◽  
Vol 21 ◽  
Author(s):  
Afza Ahmad ◽  
Irfan A. Ansari
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Flow Cytometry ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Natural Compounds ◽  
Cell Cycle Distribution ◽  
Chemotherapeutic Drugs ◽  
Cycle Progression ◽  
Cervical Cancer Cells

Background:: The carcinogenesis of uterine cervix is predominantly initiated with the consistent infection of human papilloma virus (HPV). Owing to the adverse side effects of standard chemotherapeutics in the treatment of recurrent and metastatic cervical cancer, there is a need for better and effective treatment modality. In this lieu of concern, natural compounds have proven their worthwhile potential against treatment of various carcinomas. Carvacrol is a phenolic monoterpenoid and several reports have suggested its different biological properties including antioxidant, anti-inflammatory and anticancer activity. Objective:: The objective of our present study was to investigate the effect of carvacrol on HPV18+ HeLa cervical cancer cells. Methods:: HeLa cervical cancer cells were cultured and subsequently treated with various doses of carvacrol. Cell viability was assessed via MTT assay. DAPI and Hoechst3342 staining was used to qualitatively analyzed the induced apoptosis. Reactive Oxygen Species (ROS) was estimated by DCFDA staining protocol and quantitatively estimated by flow cytometry. The cell cycle distribution and apoptosis (FITC-Annexin V assay) were analyzed by flow cytometry. Results:: The results of the present study have established that carvacrol strongly suppresses proliferation of cervical cancer cells via caspase-dependent apoptosis and abrogation of cell cycle progression. Furthermore, our preliminary study also demonstrated that carvacrol exhibits synergistic effect with chemotherapeutic drugs (5-FU and carboplatin). These initial findings implicated that natural compounds could reduce the toxic effects of chemotherapeutic drugs. Conclusion:: Therefore, this investigation affirms the anti-cancer potential of carvacrol against cervical cancer cells which could be an appendage in the prevention and treatment of cervical cancer.

scholarly journals Disruption of repressive p130–DREAM complexes by human papillomavirus 16 E6/E7 oncoproteins is required for cell-cycle progression in cervical cancer cells

2011 ◽  
Vol 92 (11) ◽  
pp. 2620-2627 ◽  
Author(s):  
Nurshamimi Nor Rashid ◽  
Rohana Yusof ◽  
Roger J. Watson
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Papillomaviruses ◽  
G1 Arrest ◽  
Cycle Progression ◽  
Hpv16 E6 ◽  
Cervical Cancer Cells ◽  
E6 And E7

Human papillomaviruses (HPVs) with tropism for mucosal epithelia are the major aetiological factors in cervical cancer. Most cancers are associated with so-called high-risk HPV types, in particular HPV16, and constitutive expression of the HPV16 E6 and E7 oncoproteins is critical for malignant transformation in infected keratinocytes. E6 and E7 bind to and inactivate the cellular tumour suppressors p53 and Rb, respectively, thus delaying differentiation and inducing proliferation in suprabasal keratinocytes to enable HPV replication. One member of the Rb family, p130, appears to be a particularly important target for E7 in promoting S-phase entry. Recent evidence indicates that p130 regulates cell-cycle progression as part of a large protein complex termed DREAM. The composition of DREAM is cell cycle-regulated, associating with E2F4 and p130 in G0/G1 and with the B-myb transcription factor in S/G2. In this study, we addressed whether p130–DREAM is disrupted in HPV16-transformed cervical cancer cells and whether this is a critical function for E6/E7. We found that p130–DREAM was greatly diminished in HPV16-transformed cervical carcinoma cells (CaSki and SiHa) compared with control cell lines; however, when E6/E7 expression was targeted by specific small hairpin RNAs, p130–DREAM was reformed and the cell cycle was arrested. We further demonstrated that the profound G1 arrest in E7-depleted CaSki cells was dependent on p130–DREAM reformation by also targeting the expression of the DREAM component Lin-54 and p130. The results show that continued HPV16 E6/E7 expression is necessary in cervical cancer cells to prevent cell-cycle arrest by a repressive p130–DREAM complex.

Flow cytometry analysis of cell population dynamics and cell cycle during HIV-1 envelope-mediated formation of syncytia in vitro

2014 ◽  
Vol 50 (5) ◽  
pp. 453-463 ◽  
Author(s):  
Israel Torres-Castro ◽  
César N. Cortés-Rubio ◽  
Guadalupe Sandoval ◽  
Edmundo Lamoyi ◽  
Carlos Larralde ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Population Dynamics ◽  
Cell Population ◽  
Flow Cytometry Analysis ◽  
Cell Population Dynamics ◽  
Hiv 1

scholarly journals The endonuclease APE1 processes miR-92b formation, thereby regulating expression of the tumor suppressor LDLR in cervical cancer cells

2019 ◽  
Vol 11 ◽  
pp. 175883591985585 ◽  
Author(s):  
Yi Sun ◽  
Yun Feng ◽  
Guiqian Zhang ◽  
Ya Xu
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cervical Carcinoma ◽  
Cell Cycle Progression ◽  
Endonuclease Activity ◽  
Cycle Progression ◽  
Cervical Cancer Cells ◽  
Novel Therapeutic

Background: The molecular mechanisms underlying cervical cancer require elucidation to identify novel therapeutic targets. Apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) is a multifunctional apurinic/apyrimidinic (AP) endonuclease that influences the transcription of many cancer-related genes via microRNome regulation. Herein, we examine the role of miR-92b-3p (hereinafter miR-92b), whose processing may be regulated by APE1, in cervical cancer progression. Methods: APE1’s processing of miR-92b from its pri-miR form was measured by a quantitative reverse transcription polymerase chain reaction (qRT-PCR)-based ratio. APE1’s endonuclease activity was measured with AP-site incision assays. APE1-DROSHA interaction was studied with immunofluorescence, confocal and proximity ligation analyses. The miR-92b’s targeting of low-density lipoprotein receptor (LDLR) was investigated with luciferase reporter assays. The miR-92b mimics and shRNA-based miR-92b silencing, as well as LDLR overexpression and short interfering RNA (siRNA)-based LDLR silencing, were employed in CaSki and SiHa cervical cancer cells. Cell proliferation and chemosensitivity to paclitaxel and cisplatin were assayed. Cell-cycle progression and apoptosis were assessed by flow cytometry. Tumor growth was studied in a murine xenograft model. Results: APE1’s endonuclease activity, via association with the DROSHA-processing complex, is necessary for processing mature miR-92b, thereby regulating expression of miR-92b’s direct target LDLR. The miR-92b promotes cell proliferation in vitro and in vivo, promotes cell-cycle progression, and reduces apoptosis and chemosensitivity. LDLR silencing recapitulated miR-92b’s transformative effects, while LDLR overexpression rescued these effects. Conclusions: APE1 enhances miR-92b processing, thereby suppressing LDLR expression and enhancing cervical carcinoma progression. Our identification of the novel APE1-miR-92b-LDLR axis improves our understanding of the complex pathogenesis of cervical carcinoma and reveals a novel therapeutic strategy for combating this disease.

Effect of the kaurenoic acid on genotoxicity and cell cycle progression in cervical cancer cells lines

2019 ◽  
Vol 57 ◽  
pp. 126-131 ◽  
Author(s):  
Silvia Maria Machado da Rocha ◽  
Plínio Cerqueira dos Santos Cardoso ◽  
Marcelo de Oliveira Bahia ◽  
Claudia do Ó Pessoa ◽  
Paulo Cardoso Soares ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Kaurenoic Acid ◽  
Cervical Cancer Cells

scholarly journals A Survey of Cell Population Dynamics

1997 ◽  
Vol 1 (1) ◽  
pp. 35-51 ◽  
Author(s):  
O. Arino ◽  
E. Sánchez
Keyword(s):  
Cell Cycle ◽  
Population Dynamics ◽  
Cell Population ◽  
Linear Models ◽  
Population Models ◽  
Cell Dynamics ◽  
Cell Population Dynamics ◽  
Non Linear

A Survey of cell-population models is presented. The so-called cell cycle is discussed, including some models which are not population models but which contribute to the better understanding proliferation of cell dynamics. Classical linear models of structured cell-population models are described with a review of classical results and a comparison between different approaches. Finally, some non-linear models are also developed.

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