Taxifolin, a natural flavonoid interacts with cell cycle regulators causes cell cycle arrest and causes tumor regression by activating Wnt/ ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-10-26

AUTHORS

Suhail Razak, Tayyaba Afsar, Asad Ullah, Ali Almajwal, Musaed Alkholief, Aws Alshamsan, Sarwat Jahan

ABSTRACT

BackgroundNew approaches for the prevention of colon cancer perseveres an essential necessity. Though, resistance to existing chemo-preventive drugs is moderately predominant in colon carcinogenesis. Taxifolin (dihydroquercetin) is a flavononol, have shown virile biological activities against few cancers. The current study was designed to investigate and equate antitumor activity of Taxifolin (TAX) in colorectal cancer cell lines and in HCT116 xenograft model in a comprehensive approach.MethodsTwo human colorectal cancer cell lines HCT116 and HT29, were used. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazoliumbromide (MMT) protocol was performed to elucidate the impact of TAX and β- catenin inhibitor (FH535) on the viability of HCT116 and HT29 cell lines. Apoptosis /cell cycle assay was performed. Data interpretation was done with a FACScan (Becton Dickinson, NJ). About 1 × 104 cells per sample were harvested. Histograms of DNA were analyzed with ModiFitLT software (verity Software House, ME, USA). Western blotting and RT-PCR were performed for protein and gene expression respectively in in vitro and in vivo.ResultsWe found that TAX induced cytotoxicity in colorectal cells in a dose-dependent manner and time dependent approach. Further, our data validated that administration of TAX to human colorectal cancer HCT116 and HT29 cells resulted in cell growth arrest, variation in molecules controlling cell cycle operative in the G2 phase of the cell cycle and apoptosis in a concentration dependent approach. Further our results concluded that TAX administration decreases expression of β-catenin gene, AKT gene and Survivin gene and protein expression in in vitro and in vivo.ConclusionOur findings proposed that targeting β-catenin gene may encourage the alterations of cell cycle and cell cycle regulators. Wnt/β-catenin signaling pathway possibly takes part in the genesis and progression of colorectal cancer cells through regulating cell cycle and the expression of cell cycle regulators. More... »

PAGES

1043

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12885-018-4959-4

DOI

http://dx.doi.org/10.1186/s12885-018-4959-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1107867516

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30367624


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67 cell cycle
68 cell cycle arrest
69 cell cycle regulators
70 cell growth arrest
71 cell lines
72 cells
73 chemo-preventive drugs
74 colon cancer
75 colon carcinogenesis
76 colorectal cancer
77 colorectal cancer cell lines
78 colorectal cancer cells
79 colorectal cells
80 comprehensive approach
81 concentration-dependent approach
82 current study
83 cycle
84 cycle arrest
85 cycle regulators
86 cytotoxicity
87 data
88 data interpretation
89 dependent approach
90 dose-dependent manner
91 drugs
92 essential necessity
93 expression
94 findings
95 flavononols
96 gene expression
97 genes
98 genesis
99 growth arrest
100 histogram
101 human colorectal cancer
102 human colorectal cancer cell lines
103 impact
104 inhibitors
105 interacts
106 interpretation
107 lines
108 manner
109 model
110 molecules
111 necessity
112 operative
113 part
114 pathway
115 phase
116 prevention
117 progression
118 protein
119 protein expression
120 protocol
121 regression
122 regulator
123 resistance
124 results
125 samples
126 software
127 study
128 survivin gene
129 tax administration
130 taxifolin
131 time-dependent approach
132 tumor regression
133 variation
134 viability
135 viability of HCT116
136 vivo
137 xenograft model
138 β-catenin
139 β-catenin gene
140 β-catenin inhibitor
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