Delicaflavone induces apoptosis via mitochondrial pathway accompanying G2/M cycle arrest and inhibition of MAPK signaling cascades in cervical cancer HeLa cells

Phytomedicine ◽  
2019 ◽  
Vol 62 ◽  
pp. 152973 ◽  
Author(s):  
Wensong Yao ◽  
Zhen Lin ◽  
Gang Wang ◽  
Shaoguang Li ◽  
Bing Chen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Mapk Signaling ◽  
Mitochondrial Pathway ◽  
Signaling Cascades ◽  
Cycle Arrest

scholarly journals Syringin exhibits anticancer effects in HeLa human cervical cancer cells by inducing apoptosis, cell cycle arrest and inhibition of cell migration

2016 ◽  
Vol 11 (4) ◽  
pp. 838 ◽  
Author(s):  
Ning Xia
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Migration ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Dependent Manner ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

<p class="Abstract">The present study was aimed at to demonstrate the antitumor effects of syringin in HeLa human cervical cancer cells. Its effects on apoptosis, cell cycle phase distribution as well as on cell migration were also examined. The effect on cell proliferation was evaluated by MTT assay, while as effects on colony formation were assessed using clonogenic assay. Syringin inhibited cancer cell growth in HeLa cells in a time-dependent as well as in a concentration-dependent manner. Syringin also led to inhibition of colony formation efficacy with complete suppression at 100 µM drug dose. Syringin could induce G2/M cell cycle arrest along with slight sub-G1 cell cycle arrest. HeLa cells began to emit red fluorescence as the dose of syringin increased from 0 µM in vehicle control to 100 µM. Syringin also inhibited cell migration in a dose-dependent manner with 100 µM dose of syringin leading to 100% inhibition of cell migration.</p><p> </p>

scholarly journals Glucocappasalin Induces G2/M-Phase Arrest, Apoptosis, and Autophagy Pathways by Targeting CDK1 and PLK1 in Cervical Carcinoma Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Guangya Xu ◽  
Xueling Yan ◽  
Zhongjia Hu ◽  
Lulu Zheng ◽  
Ke Ding ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cervical Carcinoma ◽  
Hela Cells ◽  
Carcinoma Cells ◽  
Dependent Manner ◽  
Cycle Arrest ◽  
Phase Arrest ◽  
M Phase

Glucocappasalin (GCP), a natural product derived from the seeds of Descurainia sophia (L.) Webb. ex Prantl, exhibits potential antitumor activity in HeLa cervical carcinoma cells. In this study, we investigated the anti-cervical cancer property of GCP through the induction of cell cycle arrest, apoptosis, and autophagy in vitro and in vivo, and elucidated the underlying molecular mechanisms. We demonstrated that treatment with GCP inhibited the growth of HeLa, Siha, and Ca Ski cell lines in a dose-dependent manner, with HeLa cells displaying particular sensitivity to the GCP treatment. Subsequently, the expression of cyclin-dependent kinase 1 (CDK1) and polo like kinase 1 (PLK1) were evaluated in HeLa cells using the CDK1 kinase assay kit, the fluorescence polarization assay, real-time quantitative PCR, and western blotting. Our results demonstrate that GCP could be employed to attenuate the expression of CDK1 and PLK1 in a dose- and time-dependent manner. The complementary results obtained by flow cytometry and western blotting allowed us to postulate that GCP may exhibit its antitumor effects by inducing G2/M cell cycle arrest. Moreover, HeLa cells treated with GCP exhibited a loss in mitochondrial membrane potential, together with the activation of caspases 3 and 9, and poly ADP-ribose polymerase (PARP). Additionally, we found that GCP could increase the formation of acidic vesicular organelles (AVOs), as well as the levels of Beclin1, LC3-II, p62, and Atg5 proteins in HeLa cells. Further studies indicated that GCP triggered autophagy via the suppression of the PI3K/AKT/mTOR signaling pathways. The autophagy inhibitor 3-methyladenine (3-MA) was used to determine whether autophagy affects the apoptosis induced by GCP. Interestingly, the inhibition of autophagy attenuated apoptosis. In vivo anti-tumor experiments indicated that GCP (60 mg/kg, i.p.) markedly reduced the growth of HeLa xenografts in nude mice without apparent toxicity. Taken together, we demonstrate that GCP induces cell cycle G2/M-phase arrest, apoptosis, and autophagy by acting on the PI3K/AKT/mTOR signaling pathways in cervical carcinoma cells. Thus, GCP may represent a promising agent in the eradication of cervical cancer.

scholarly journals Anticancer Effect of Natural Product Sulforaphane by Targeting MAPK Signal through miRNA-1247-3p in Human Cervical Cancer Cells

2020 ◽  
Vol 11 (1) ◽  
pp. 7943-7972
Keyword(s):  
Cervical Cancer ◽  
Flow Cytometry ◽  
Western Blot ◽  
Hela Cells ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Cell Counting ◽  
Hela Cell Lines ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis

The prognosis of cervical cancer remains poor. Sulforaphane, an active ingredient from cruciferous plants, has been identified as a potential anticancer agent in various cancers. However, there is little information about its effect on cervical cancer. Here, we conducted a present study to uncover the effect and the potential mechanisms of sulforaphane on cervical cancer. HeLa cells were treated with sulforaphane, and cell proliferation and apoptosis were assessed by Cell Counting Kit-8, Western blot, flow cytometry, and immunofluorescence. Then, next-generation sequencing (NGS) and bioinformatics tools were used to analyze mRNA-seq, miRNA-seq, and potential pathways. Finally, qRT-PCR, Cell Counting Kit-8, flow cytometry, small RNAs analysis, and Western blot were performed to evaluate the biological function of miR1247-3p and MAPK pathway in HeLa cell lines. Sulforaphane significantly suppressed the viability and induced apoptosis of HeLa cells. NGS and bioinformatics analysis showed sulforaphane exerted its anti-tumor activities through miR1247-3p and the MAPK signaling pathway. Further analysis suggested that sulforaphane could activate MAPK pathway via down-regulating the expression of miR-1247-3p. Sulforaphane inhibited proliferation and promoted apoptosis of HeLa cells via down-regulation of miR-1247-3p and activating the MAPK pathway. These findings provide preliminary experimental evidence for the treatment of cervical cancer with sulforaphane.

scholarly journals Ethanol Extract of Croton Kongensis Promotes Cell Cycle Arrest and Consequently Inhibits Anchorage-Independent Growth of Cervical Cancer Hela Cells

2021 ◽  
Vol 37 (3) ◽  
Author(s):  
Nguyen Thi Bich Loan ◽  
Nguyen Lai Thanh ◽  
Pierre Duez ◽  
Nguyen Dinh Thang
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Ethanol Extract ◽  
Soft Agar ◽  
Anticancer Activities ◽  
Anchorage Independent Growth ◽  
Cycle Arrest ◽  
G2 Phase

Extracts from Croton kongenis present anticancer activities on various cancers. However, there is no research conducted to investigate the effects of Croton kongenis extracts on cervical cancer as well as on zebrafish. In this study, we demonstrated that Croton kongenis ethanol extract expressed high toxicity to cervical cancer Hela cells with an IC50 dose of 20.4 µg/mL and to zebrafish embryos with malformations, lethality and hatching inhibition at 72-hpf at effective dose of 125 µg/mL. Interestingly, treatment with Croton kongenis ethanol extract caused cell-cycle-arrest at the G2 phase. Particularly, percentages of Croton kongenis ethanol extract-treated cells in G1, S, G2/M were 70%, 6% and 23%, while percentages of control cells in G1, S, G2/M were 65%, 15% and 18%, respectively. Consistent with cell-cycle-arrest, the expressions of CDKN1A, CDNK2A and p53 in Croton kongenis ethanol extract-treated cells were up-regulated 2.0-, 1.65- and 1.8-fold, respectively. Significantly, treatment with Croton kongenis ethanol extract inhibited anchorage-independent growth of Hela cells; the number of colonies formed in soft-agar of Croton kongenis ethanol extract-treated cells was only one-fourth of that of control cells. In conclusion, we suggest that Croton kongenis ethanol extract could be able to use as a traditional medicine for treatment of cervical cancer.

scholarly journals Coix lacryma-jobi var. ma-yuen Stapf sprout extract induces cell cycle arrest and apoptosis in human cervical carcinoma cells

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Eun Suk Son ◽  
Se-Hee Kim ◽  
Young Ock Kim ◽  
Young Eun Lee ◽  
Sun Young Kyung ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Flow Cytometric Analysis ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Cycle Arrest ◽  
Flow Cytometric

Abstract Background Cervical cancer is the second-leading cause of cancer-related mortality in females. Coix lacryma-jobi L. var. ma-yuen (Rom.Caill.) Stapf ex Hook. f. is the most widely recognized medicinal herb for its remedial effects against inflammation, endocrine system dysfunctions, warts, chapped skin, rheumatism, and neuralgia and is also a nourishing food. Methods To investigate the activity of Coix lacryma-jobi sprout extract (CLSE) on cell proliferation in human cervical cancer HeLa cells, we conducted a Cell Counting Kit-8 (CCK-8) assay. Flow-cytometric analysis and western blot analysis were performed to verify the effect of CLSE on the regulation of the cell cycle and apoptosis in HeLa cells. Results We observed that CLSE significantly inhibited cell proliferation. Furthermore, CLSE dose-dependently promoted cell cycle arrest at the sub-G1/ S phase in HeLa cells, as detected by bromodeoxyuridine (BrdU) staining. The cell-cycle-arrest effects of CLSE in HeLa cells were associated with downregulation of cyclin D1 and cyclin-dependent kinases (CDKs) 2, 4, and 6. Moreover, CLSE induced apoptosis, as determined by flow-cytometric analysis and nuclear DNA fragmentation with Annexin V/propidium iodide (PI) and 4′6′-diamidino-2-phenylindole (DAPI) staining. Induction of apoptosis by CLSE was involved in inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) and upregulation of the apoptotic proteins p53, cleaved poly (ADP-ribose) polymerase (PARP), cleaved caspase-3, and cleaved caspase-8. Finally, we observed that CLSE inactivated the phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) pathways. Conclusions CLSE causes cell cycle arrest and apoptotic cell death through inactivation of the PI3K/AKT pathway in HeLa cells, suggesting it is a viable therapeutic agent for cervical cancer owing to its anticancer effects.

scholarly journals Polypeptide Fraction fromArca subcrenataInduces Apoptosis and G2/M Phase Arrest in HeLa Cells via ROS-Mediated MAPKs Pathways

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xianjing Hu ◽  
Zhang Zhang ◽  
Ting Liu ◽  
Liyan Song ◽  
Jianhua Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Underlying Mechanism ◽  
Cyclin B1 ◽  
Mitochondrial Pathway ◽  
Dependent Manner ◽  
Phase Arrest ◽  
M Phase ◽  
Induced Apoptosis ◽  
High Level

Arca subcrenatais documented in the literature of marine Traditional Chinese Medicine. Polypeptide fraction fromA. subcrenata, coded as P2, was demonstrated to possess significant antitumor activity in our previous study. However, the underlying mechanism remains undefined. The present study was carried out to investigate the underlying antitumor mechanism of P2 in human cervical cancer HeLa cells by MTT, FCM, LSCM, and western blot assays. The results revealed that P2 significantly induced apoptosis of HeLa cells in a concentration- and time-dependent manner. High level of ROS was provoked by P2, which was in turn responsible for induction of apoptosis through activation of intrinsic mitochondrial pathway and JNK1/2, p38 MAPK pathways, as well as inhibition of ERK1/2 pathway, as evidenced by the abrogation of P2’s effect on HeLa cells preincubated with the ROS scavenger NAC. P2 also was observed to display significant effect on G2/M phase arrest by downregulating the expression of cyclin B1/cdc2 complex and upregulating the expression of p21. These findings demonstrate that P2 induces apoptosis and G2/M phase arrest in HeLa cells through ROS-mediated MAPKs pathways, suggesting that P2 would be worth investigating as a promising agent within the scope of marine drugs for treatment of cervical cancer.

Effects of Ginkgolide B on the Proliferation and Apoptosis of Cervical Cancer Cells

2020 ◽  
Vol 18 (3) ◽  
pp. 227-232
Author(s):  
Xu Yiling ◽  
Ma Qingfeng ◽  
Chen Dejun ◽  
Yin Qing ◽  
Zhang Wei
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Ginkgo Biloba ◽  
Biological Activities ◽  
Invasive Cervical Cancer ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Ginkgolide B ◽  
Cycle Arrest ◽  
Cervical Cancer Cells

Cervical cancer is the fourth most common cancer among women worldwide. The treatment of cervical cancer mainly focused on surgery and radiotherapy, whereas the prognosis of invasive cervical cancer is still low. Ginkgo biloba is an ancient medicinal plant that has been used for decades to treat ischemic strokes and cognitive decline. Ginkgolide B, an active ingredient extracted from Ginkgo biloba, has multiple biological activities such as antioxidant, anti-apoptotic, and anti-inflammatory effects. Ginkgolide B has been found to have anti-tumor effects and inhibits the progression of multiple types of cancers. However, its potential role in cervical cancer is still unclear. In this study, we found that ginkgolide B suppresses the proliferation of cervical cancer cells in a dose-dependent manner. Ginkgolide B also induces cell cycle arrest and stimulates cell apoptosis by modulating the MAPK signaling pathway. We, therefore, present a novel and promising anti-tumor drug for the treatment of cervical cancer.

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