The flavonoid quercetin induces cell cycle arrest and mitochondria-mediated apoptosis in human cervical cancer (HeLa) cells through p53 induction and NF-κB inhibition

2010 ◽  
Vol 649 (1-3) ◽  
pp. 84-91 ◽  
Author(s):  
R. Vidya Priyadarsini ◽  
R. Senthil Murugan ◽  
S. Maitreyi ◽  
K. Ramalingam ◽  
D. Karunagaran ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Cycle Arrest ◽  
Flavonoid Quercetin ◽  
Human Cervical Cancer

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 Bersaldegenin-1,3,5-orthoacetate induces caspase-independent cell death, DNA damage and cell cycle arrest in human cervical cancer HeLa cells

2021 ◽  
Vol 59 (1) ◽  
pp. 54-65
Author(s):  
Justyna Stefanowicz-Hajduk ◽  
Magdalena Gucwa ◽  
Barbara Moniuszko-Szajwaj ◽  
Anna Stochmal ◽  
Anna Kawiak ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Cycle Arrest ◽  
Human Cervical Cancer

scholarly journals Securinine from Phyllanthus glaucus Induces Cell Cycle Arrest and Apoptosis in Human Cervical Cancer HeLa Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0165372 ◽  
Author(s):  
Justyna Stefanowicz-Hajduk ◽  
Barbara Sparzak-Stefanowska ◽  
Mirosława Krauze-Baranowska ◽  
J. Renata Ochocka
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Cycle Arrest ◽  
Human Cervical Cancer

scholarly journals Anticancer activity of isomultiflorenol against human cervical cancer cells due to G2/M cell cycle arrest, autophagy and mitochondrial mediated apoptosis

2020 ◽  
Vol 19 (7) ◽  
pp. 1423-1428
Author(s):  
Juan Li ◽  
Yuanyuan Chen
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Hela Cells ◽  
Cycle Arrest ◽  
M Phase ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Purpose: To determine the anticancer effect of a pentacyclic triterpenoid, isomultiflorenol, against human cervical cancer.Methods: The proliferation of cancer cells was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyl tetrazolium bromide (MTT) assay. Cell viability was measured with colony forming assay, while flow cytometry was used to study phase distribution in cancer cell mitosis. Electron microscopy was employed for the determination of autophagy induction in the cancer cells, while western blotting was used to assay protein expressions.Results: Isomultiflorenol significantly (p < 0.05) inhibited the proliferation and viability of cervical cancer cells in a concentration-dependent manner. The IC50 of isomultiflorenol was 10 μM for HeLa cells, and 90 μM for normal EV304 cells. The anti-proliferative effects were exerted as a result of arrest of HeLa cells at G2/M phase. The G2/M phase cells increased from 10.34 % in control to 30.21 % on treatment with 20 μM isomultiflorenol. Furthermore, administration of isomultiflorenol led to induction of cancer cell autophagy via mitochondrial apoptotic signaling.Conclusion: Isomultiflorenol inhibits human cervical cancer cells in vitro by inducing cell cycle arrest and autophagy. Thus, it is a potential lead molecule in the development of cervical cancer chemotherapy. Keywords: Cervical cancer, Terpenoids, Isomultiflorenol, Autophagy, Cell cycle arrest, Apoptosis

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.

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