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

<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>

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The neem limonoids azadirachtin and nimbolide induce cell cycle arrest and mitochondria-mediated apoptosis in human cervical cancer (HeLa) cells

Free Radical Research ◽

10.3109/10715761003692503 ◽

2010 ◽

Vol 44 (6) ◽

pp. 624-634 ◽

Cited By ~ 84

Author(s):

R. Vidya Priyadarsini ◽

R. Senthil Murugan ◽

P. Sripriya ◽

D. Karunagaran ◽

S. Nagini

Keyword(s):

Cell Cycle ◽

Cervical Cancer ◽

Cell Cycle Arrest ◽

Hela Cells ◽

Induce Cell Cycle Arrest ◽

Cycle Arrest ◽

Human Cervical Cancer

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

European Journal of Pharmacology ◽

10.1016/j.ejphar.2010.09.020 ◽

2010 ◽

Vol 649 (1-3) ◽

pp. 84-91 ◽

Cited By ~ 224

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

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Cordyceps cicadae polysaccharides inhibit Human cervical cancer Hela cells proliferation via Apoptosis and Cell Cycle Arrest

Food and Chemical Toxicology ◽

10.1016/j.fct.2021.111971 ◽

2021 ◽

pp. 111971

Author(s):

Jiao Xu ◽

Zhi-Cheng Tan ◽

Zhong-Yuan Shen ◽

Xing-Jia Shen ◽

Shun-Ming Tang

Keyword(s):

Cell Cycle ◽

Cervical Cancer ◽

Cell Cycle Arrest ◽

Hela Cells ◽

Cycle Arrest ◽

Cordyceps Cicadae ◽

Human Cervical Cancer

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

PLoS ONE ◽

10.1371/journal.pone.0165372 ◽

2016 ◽

Vol 11 (10) ◽

pp. e0165372 ◽

Cited By ~ 10

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

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Achillea millefolium L. ethyl acetate fraction induces apoptosis and cell cycle arrest in human cervical cancer (HeLa) cells

Annals of Agricultural Sciences ◽

10.1016/j.aoas.2020.03.003 ◽

2020 ◽

Vol 65 (1) ◽

pp. 42-48 ◽

Cited By ~ 4

Author(s):

Doha H. Abou Baker

Keyword(s):

Cell Cycle ◽

Cervical Cancer ◽

Ethyl Acetate ◽

Cell Cycle Arrest ◽

Hela Cells ◽

Ethyl Acetate Fraction ◽

Achillea Millefolium ◽

Cycle Arrest ◽

Human Cervical Cancer

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

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v19i7.13 ◽

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

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RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response

International Journal of Genomics ◽

10.1155/2013/271347 ◽

2013 ◽

Vol 2013 ◽

pp. 1-12 ◽

Cited By ~ 22

Author(s):

Toshinori Ozaki ◽

Akira Nakagawara ◽

Hiroki Nagase

Keyword(s):

Cell Cycle ◽

Dna Damage ◽

Cell Death ◽

Cell Cycle Arrest ◽

Dna Damage Response ◽

Apoptotic Cell ◽

Genetic Alterations ◽

Apoptotic Cell Death ◽

Cycle Arrest ◽

Damage Response

A proper DNA damage response (DDR), which monitors and maintains the genomic integrity, has been considered to be a critical barrier against genetic alterations to prevent tumor initiation and progression. The representative tumor suppressor p53 plays an important role in the regulation of DNA damage response. When cells receive DNA damage, p53 is quickly activated and induces cell cycle arrest and/or apoptotic cell death through transactivating its target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death such asp21WAF1,BAX, andPUMA. Accumulating evidence strongly suggests that DNA damage-mediated activation as well as induction of p53 is regulated by posttranslational modifications and also by protein-protein interaction. Loss of p53 activity confers growth advantage and ensures survival in cancer cells by inhibiting apoptotic response required for tumor suppression. RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and/or tumorigenesis. In this review, we describe a background of p53 and a functional collaboration between p53 and RUNX family in response to DNA damage.

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