scholarly journals Deoxyelephantopin from Elephantopus scaber Inhibits HCT116 Human Colorectal Carcinoma Cell Growth through Apoptosis and Cell Cycle Arrest

Molecules ◽  
2016 ◽  
Vol 21 (3) ◽  
pp. 385 ◽  
Author(s):  
Chim Chan ◽  
Gomathi Chan ◽  
Khalijah Awang ◽  
Habsah Abdul Kadir
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cell ◽  
Cycle Arrest ◽  
Human Colorectal Carcinoma Cell ◽  
Elephantopus Scaber ◽  
Human Colorectal Carcinoma

scholarly journals Induction of p53-Independent Apoptosis and G1 Cell Cycle Arrest by Fucoidan in HCT116 Human Colorectal Carcinoma Cells

Marine Drugs ◽  
2017 ◽  
Vol 15 (6) ◽  
pp. 154 ◽  
Author(s):  
Hye Park ◽  
Shin-Hyung Park ◽  
Jin-Woo Jeong ◽  
Dahye Yoon ◽  
Min Han ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Human Colorectal Carcinoma

scholarly journals Lentivirus-mediated LIGHT overexpression inhibits human colorectal carcinoma cell growth in vitro and in vivo

2013 ◽  
Vol 6 (4) ◽  
pp. 927-932 ◽  
Author(s):  
HAIBO WANG ◽  
ZHUANG YU ◽  
SHIHAI LIU ◽  
XIANGPING LIU ◽  
AIHUA SUI ◽  
...  
Keyword(s):  
Cell Growth ◽  
Colorectal Carcinoma ◽  
Carcinoma Cell ◽  
Human Colorectal Carcinoma Cell ◽  
Human Colorectal Carcinoma

siRNA-Mediated Silencing of HMGA2 Induces Apoptosis and Cell Cycle Arrest in Human Colorectal Carcinoma

2016 ◽  
Vol 48 (2) ◽  
pp. 156-163 ◽  
Author(s):  
Sahar Esmailzadeh ◽  
Behzad Mansoori ◽  
Ali Mohammadi ◽  
Dariush Shanehbandi ◽  
Behzad Baradaran
Keyword(s):  
Cell Cycle ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Human Colorectal Carcinoma

scholarly journals Dimethylfumarate Inhibits Colorectal Carcinoma Cell Proliferation: Evidence for Cell Cycle Arrest, Apoptosis and Autophagy

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1329 ◽  
Author(s):  
Kaluzki ◽  
Hailemariam-Jahn ◽  
Doll ◽  
Kaufmann ◽  
Balermpas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Carcinoma Cell ◽  
Human Colon ◽  
G1 Phase ◽  
Cycle Arrest

Recent studies have proven that Dimethylfumarate (DMF) has a marked anti-proliferative impact on diverse cancer entities e.g., on malignant melanoma. To explore its anti-tumorigenic potential, we examined the effects of DMF on human colon carcinoma cell lines and the underlying mechanisms of action. Human colon cancer cell line HT-29 and human colorectal carcinoma cell line T84 were treated with or without DMF. Effects of DMF on proliferation, cell cycle progression, and apoptosis were analyzed mainly by Bromodeoxyuridine (BrdU)- and Lactatdehydrogenase (LDH)assays, caspase activation, flowcytometry, immunofluorescence, and immunoblotting. In addition, combinational treatments with radiation and chemotherapy were performed. DMF inhibits cell proliferation in both cell lines. It was shown that DMF induces a cell cycle arrest in G0/G1 phase, which is accompanied by upregulation of p21 and downregulation of cyclin D1 and Cyclin dependent kinase (CDK)4. Furthermore, upregulation of autophagy associated proteins suggests that autophagy is involved. In addition, the activation of apoptotic markers provides evidence that apoptosis is involved. Our results show that DMF supports the action of oxaliplatin in a synergetic manner and failed synergy with radiation. We demonstrated that DMF has distinct antitumorigenic, cell dependent effects on colon cancer cells by arresting cell cycle in G0/G1 phase as well as activating both the autophagic and apoptotic pathways and synergizes with chemotherapy.

LYG-202 inhibits the proliferation of human colorectal carcinoma HCT-116 cells through induction of G1/S cell cycle arrest and apoptosis via p53 and p21WAF1/Cip1 expression

2011 ◽  
Vol 89 (3) ◽  
pp. 287-298 ◽  
Author(s):  
Wei Liu ◽  
Qinsheng Dai ◽  
Na Lu ◽  
Libin Wei ◽  
Jun Ha ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Down Regulation ◽  
Transfected Cells ◽  
Cycle Arrest ◽  
Hct 116 ◽  
Human Colorectal Carcinoma ◽  
Hct 116 Cells

We recently established that LYG-202, a new flavonoid with a piperazine substitution, exerts an anti-tumor effect in vivo and in vitro. In the present study, we demonstrate that LYG-202 induces G1/S phase arrest and apoptosis in human colorectal carcinoma HCT-116 cells. Data showed that the blockade of the cell cycle was associated with increased p21WAF1/Cip1 and Rb levels and reduced expression of cyclin D1, cyclin E, and CDK4. Moreover, PARP cleavage, activation of caspase-3, caspase-8, and caspase-9, and an increased ratio of Bax/Bcl-2 were detected in LYG-202-induced apoptosis. Additionally, activation of p53 resulted in the up-regulation of its downstream targets PUMA and p21WAF1/Cip1, as well as the down-regulation of its negative regulator MDM2, suggesting that the p53 pathway may play a crucial role in LYG-202-induced cell cycle arrest and apoptosis. Furthermore, siRNA knockdown of p53 attenuated the G1 cell cycle arrest and apoptosis induced by LYG-202, as the effects of LYG-202 on up-regulation of p21WAF1/Cip1 and down-regulation of Bcl-2 and pro-caspase-3 were partly inhibited in p53 siRNA transfected cells compared with control siRNA transfected cells. Collectively, these data indicate that LYG-202 exerts its anti-tumor potency by activating the p53–p21 pathway for G1/S cell cycle arrest and apoptosis in colorectal cancer cells.

Antitumour Activity of Muricatacin Isomers and its Derivatives in Human Colorectal Carcinoma Cell HCT116

2020 ◽  
Vol 20 (2) ◽  
pp. 254-263 ◽  
Author(s):  
Wencong Wang ◽  
Rui Zhang ◽  
Jinxing Wang ◽  
Jun Tang ◽  
Mingan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Carcinoma Cell ◽  
Early Stage ◽  
Antitumour Activity ◽  
Caspase 9 ◽  
Cycle Arrest ◽  
Hct116 Cells

Background and Purpose: Colorectal cancer is one of the leading causes of cancer-related death in elderly people. The natural product muricatacin is an important member of the γ-lactone family, and it has exhibited antitumour activity in multiple cancer cell lines; however, the antitumour activities of muricatacin stereoisomers and their derivatives in colorectal cancer cells have not yet been systematically explored. Methods: The colorectal carcinoma cell line HCT116 was investigated in this study. Cell proliferation was assessed by MTT assay or crystal violet staining. Cell cycle arrest and cell apoptosis were evaluated by flow cytometry assay. The expression levels of p53, p21, cyclin E, cyclin D1, caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9 and LC3B were measured using western blot analysis. Autophagy induced by M2 was monitored by immunofluorescence assay with an antibody against LC3B. Results: Cell proliferation assays showed that both naturally occurring muricatacin (M4) and its synthetic stereoisomer (M2) are potent cell growth inhibitors in HCT116 cells, with IC50 values of 79.43 and 83.17μM, respectively; these values are much lower than those of the other two isomers, M1 and M3, and those of the sixmembered lactone analogues. The flow cytometry analysis revealed that M2 and M4 induced significant cell cycle arrest during G0/G1 phase and caused relatively low apoptosis rates in HCT116 cells. Further analysis indicated that M2 caused p53-independent p21 induction and cyclin E/cyclin D1 downregulation. In addition, M2 also markedly induced autophagy in the early stage of administration. Conclusions: Our results suggested that muricatacins possess potent antitumour activity against the colorectal carcinoma cell line HCT116 through inducing G0/G1 phase cell cycle arrest and autophagy in the early stage of administration.

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