scholarly journals Differential expression of volume‐regulated anion channels during cell cycle progression of human cervical cancer cells

2000 ◽  
Vol 529 (2) ◽  
pp. 385-394 ◽  
Author(s):  
Meng‐Ru Shen ◽  
Guy Droogmans ◽  
Jan Eggermont ◽  
Thomas Voets ◽  
J. Clive Ellory ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cancer Cells ◽  
Differential Expression ◽  
Cell Cycle Progression ◽  
Anion Channels ◽  
Cycle Progression ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

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.

Amiodarone’s major metabolite, desethylamiodarone, induces apoptosis in human cervical cancer cells

2018 ◽  
Vol 96 (10) ◽  
pp. 1004-1011 ◽  
Author(s):  
Zita Bognar ◽  
Katalin Fekete ◽  
Rita Bognar ◽  
Aliz Szabo ◽  
Reka A. Vass ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Hela Cell ◽  
Cancer Cells ◽  
Hela Cells ◽  
Dead Cell ◽  
Dependent Manner ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Previously, we found that desethylamiodarone (DEA) may have therapeutic potentiality in bladder cancer. In this study, we determined its effects on human cervical cancer cells (HeLa). Cell viability was evaluated by Muse Cell Count & Viability Assay; cell apoptosis was detected by Muse Annexin V & Dead Cell Assay. Cell cycle was flow cytometrically determined by Muse Cell Cycle Kit and the morphological changes of the cells were observed under a fluorescence microscope after Hoechst 33342 staining. The changes in the expression levels of apoptosis-related proteins in the HeLa cells were assessed by immunoblot. Our results showed that DEA significantly inhibited the proliferation and viability of HeLa cells and induced apoptosis in vitro in dose-dependent and also in cell cycle-dependent manner because DEA induced G0/G1 phase arrest in the HeLa cell line. We found that DEA treatment downregulated the expression of phospho-Akt and phospho-Bad. In addition, DEA could downregulate expression of Bcl-2, upregulate Bax, and induce cytochrome c release. Our results indicate that DEA might have significance as an anti-tumor agent against human cervical cancer.

scholarly journals Anticancer Potential of Green Synthesized Silver Nanoparticles Using Extract of Nepeta deflersiana against Human Cervical Cancer Cells (HeLA)

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Ebtesam S. Al-Sheddi ◽  
Nida N. Farshori ◽  
Mai M. Al-Oqail ◽  
Shaza M. Al-Massarani ◽  
Quaiser Saquib ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Silver Nanoparticles ◽  
Cell Death ◽  
Cancer Cells ◽  
Dependent Manner ◽  
Cytotoxic Response ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

In this study, silver nanoparticles (AgNPs) were synthesized using aqueous extract of Nepeta deflersiana plant. The prepared AgNPs (ND-AgNPs) were examined by ultraviolet-visible spectroscopy, Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), transmission electron microscopy (TEM), scanning electron microscope (SEM), and energy dispersive spectroscopy (EDX). The results obtained from various characterizations revealed that average size of synthesized AgNPs was 33 nm and in face-centered-cubic structure. The anticancer potential of ND-AgNPs was investigated against human cervical cancer cells (HeLa). The cytotoxic response was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), neutral red uptake (NRU) assays, and morphological changes. Further, the influence of cytotoxic concentrations of ND-AgNPs on oxidative stress markers, reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), cell cycle arrest and apoptosis/necrosis was studied. The cytotoxic response observed was in a concentration-dependent manner. Furthermore, the results also showed a significant increase in ROS and lipid peroxidation (LPO), along with a decrease in MMP and glutathione (GSH) levels. The cell cycle analysis and apoptosis/necrosis assay data exhibited ND-AgNPs-induced SubG1 arrest and apoptotic/necrotic cell death. The biosynthesized AgNPs-induced cell death in HeLA cells suggested the anticancer potential of ND-AgNPs. Therefore, they may be used to treat the 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.

Sign in / Sign up

Export Citation Format

Share Document