scholarly journals Essential Oil from Zingiber ottensii Induces Human Cervical Cancer Cell Apoptosis and Inhibits MAPK and PI3K/AKT Signaling Cascades

Plants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1419
Author(s):  
Jirapak Ruttanapattanakul ◽  
Nitwara Wikan ◽  
Kittinan Chinda ◽  
Thanathorn Jearanaikulvanich ◽  
Napatsorn Krisanuruks ◽  
...  

Zingiber ottensii (ZO) is a local plant in Thailand and has been used as a Thai traditional therapy for many conditions. ZO has been reported to exhibit many pharmacological effects, including anti-cancer activity. Nevertheless, its anti-cancer effects explored at the signaling level have not been elucidated in cervical cancer, which is one of the leading causes of fatality in females. We discovered that the essential oil of ZO significantly increased the apoptosis of human cervical cancer cells (HeLa) after 24 h of treatment in a concentration-dependent manner. Our data also clearly demonstrated that ZO essential oil reduced IL-6 levels in the culture supernatants of the cancer cells. Moreover, Western blot analysis clearly verified that cells were induced to undergo apoptotic death via caspase activation upon treatment with ZO essential oil. Interestingly, immunofluorescence studies and Western blot analyses showed that ZO essential oil suppressed epidermal growth factor (EGF)-induced pAkt and pERK1/2 signaling pathway activation. Together, our study demonstrates that ZO essential oil can reduce the proliferation and survival signaling of HeLa cervical cancer cells. Our study provides convincing data that ZO essential oil suppresses the growth and survival of cervical cancer cells, and it may be a potential choice for developing an anti-cancer agent for treating certain cervical cancers.

2021 ◽  
Vol 18 (7) ◽  
pp. 1455-1460
Author(s):  
Songnian Liang ◽  
Linlin Liu

Purpose: To investigate the anticancer effects of sparteine against human cervical cancer. Methods: Cell viability was determined by CCK8 assay, while 4′, 6-diamidino-2-phenylindole (DAPI) staining was used for determination of apoptosis. Cell cycle analysis was done with flow cytometry, while cell invasion was monitored using Transwell invasion assays. Protein expressions were determined using Western blotting. Results: The results revealed that sparteine inhibited the viability of cervical cancer cells with halfmaximal inhibitory concentration (IC50) ranging from 10 to 25 µM. Sparteine exerted more profound antiproliferative effects on DoTc2 cells, with IC50 of 10 µM. However, minimal cytotoxicity was observed in normal cervical cells, as evident from the IC50 of 80 µM. Sparteine triggered the generation of ROS and apoptotic cell death in DoTc2 cells. The induction of apoptosis was accompanied by upregulation of Bax expression and downregulation of Bcl-2 expression. Sparteine caused arrest of DoTc2 cells at the G0/G1 phase of the cell cycle, and suppressed the expressions of cyclin A and cyclin B1. Transwell assay data showed that sparteine decreased the invasion ability of DoTc2 cells. Sparteine also inhibited the phosphorylation of VGFR2 in a concentration-dependent manner. Conclusion: Sparteine exhibits significant anticancer activity and may prove beneficial in cervical cancer chemotherapy.


2018 ◽  
Vol 96 (10) ◽  
pp. 1004-1011 ◽  
Author(s):  
Zita Bognar ◽  
Katalin Fekete ◽  
Rita Bognar ◽  
Aliz Szabo ◽  
Reka A. Vass ◽  
...  

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.


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 ◽  
...  

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.


2015 ◽  
Vol 11 (1) ◽  
pp. 43
Author(s):  
Shu-Hong Hu ◽  
Hui Yu ◽  
Xue-Qin Gong ◽  
Ying-Hong Zhang

<p class="Abstract">The aim of the current investigation was to design, synthesize and demonstrate the anticancer and apoptotic activity of trifluoromethyl-phenyl-triazolyl derivative of beta-bisabolol (TTB) in ME-180 human cervical cancer cells.  MTT and clonogenic assays were used to evaluate the cell viability and colony formation tendencies of the cells respectively. Phase contrast and fluorescence microscopic investigations were used to evaluate the effect of TTB on cellular morphology and apoptosis. Flow cytometric analysis using fluorescent CM-DCFH2-DA were used to study the effect of TTB on reactive oxygen species (ROS) formation. The results revealed that TTB significantly inhibited the proliferation of ME-180 human cervical cancer cells in a time-dependent as well as dose-dependent manner. TTB has the capacity to inhibit both anchorage dependent as well as anchorage independent growth of ME-180 cervical cancer cells. TTB-treated cells revealed chromatin condensation, fragmented nuclei and nuclear shrinkage. A 3-fold increase of ROS production was seen after 72 μM TTB treatment.</p><p><strong><br /></strong></p><p><strong>VIDEO CLIPS</strong></p><p><a href="https://www.youtube.com/v/9yrPL3uy6Ls">Phase contrast microscopic study:</a>  2 min</p><p> </p>


2013 ◽  
Vol 41 (05) ◽  
pp. 1169-1180 ◽  
Author(s):  
Pei-Yu Yang ◽  
Dan-Ning Hu ◽  
Fu-Shing Liu

Antrodia camphorata is a Chinese herb indigenous to Taiwan. Previous reports demonstrated that it could induce apoptosis in some cancer cells. The purpose of this study was to investigate the apoptotic effect of the crude extract of A. camphorata in cervical cancer cells. Two human cervical cancer cell lines, HeLa and C-33A, were treated with extract of A. camphorata (10–1000 μg/mL). We found that A. camphorata extract was cytotoxic to both cervical cancer cells in a dose- and time-dependent manner as examined by MTT assay. Treatment with A. camphorata extract at 400 μg/mL induced a 2.3- and 4.4-fold increase in oligonucleosome formation from the cleaved chromosomal DNA in HeLa and C-33A cells, respectively. A. camphorata extract also activated caspase-3, -8, and -9 activities and increased the cytosolic level of cytochrome c in both cell lines as the dosage increased. Furthermore, A. camphorata extract increased expressions of Bak, Bad and Bim, while decreasing expressions of Bcl-2 and Bcl-xL of the Bcl-2 family proteins in HeLa and C-33A cells. The expression of IAP proteins, XIAP and survivin, was also decreased in both cervical cancer cells after treatment with A. camphorata. Our in vitro study suggests that A. camphorata is cytotoxic to cervical cancer cells through both extrinsic and intrinsic apoptotic mechanisms. It could be used as a novel phytotherapeutic agent or auxiliary therapy in the treatment of cervical cancer.


2021 ◽  
Vol 17 (1) ◽  
pp. 39-43
Author(s):  
Nurul Hidayah Wahab ◽  
Nor Fazila Che Mat

Baicalein was proved to have an apoptotic effect on a wide range of cancer cells in numerous studies. In this study, the apoptotic effect of baicalein-rich fraction from Oroxylum indicum leaves on human cervical cancer cells (SiHa and HeLa) were investigated. In this case, BRF-induced cell death was regulated by the activation of JNK/p38 and deactivation of ERK. Apart from that, BRF was able to trigger mitochondrial-mediated apoptosis pathway by downregulating Bcl-2 as well as upregulating Bax, caspase-9 and caspase-3. Indeed, MAPK transduction was found to be involved in BRF action in modulating mitochondrial Bcl-2 family, Bcl-2 and Bax. In SiHa cells, ERK and p38 pathway regulated BRF stimulation on mitochondrial-mediated pathway. Yet, BRF-induced this apoptosis pathway in ERK/JNK/p38-dependent manner in HeLa cells. Therefore, BRF induced and augmented the cell death of human cervical cancer cells through MAPK transduction.


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