scholarly journals Knockdown of Forkhead box A1 suppresses the tumorigenesis and progression of human colon cancer cells through regulating the phosphatase and tensin homolog/Akt pathway

2020 ◽  
Vol 48 (12) ◽  
pp. 030006052097145
Author(s):  
Jie Pan ◽  
Zongbin Xu ◽  
Meifang Xu ◽  
Xiaoyan Lin ◽  
Bingqiang Lin ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Human Colon ◽  
Migration And Invasion ◽  
Human Colon Cancer ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Forkhead Box ◽  
Mrna And Protein Expression ◽  
Cancer Tissues ◽  
Foxa1 Expression

Background This study aimed to evaluate the role and the underlying mechanisms of Forkhead box A1 (encoded by FOXA1) in colon cancer. Methods We analyzed FOXA1 mRNA and protein expression in colon cancer tissues and cell lines. We also silenced FOXA1 expression in HCT116 and SW480 cells to evaluate the effects on cell proliferation, cell cycle, migration, and invasion by using MTT, colony formation, flow cytometry, and the Transwell assay, respectively. Results FOXA1 immunostaining was higher in colon cancer tissues than adjacent healthy tissues. FOXA1 mRNA and protein expression was significantly increased in human colon cancer cells compared with a normal colonic cell line. FOXA1 expression was also significantly higher in colorectal cancer tissues from TCGA data sets and was associated with worse prognosis in the R2 database. FOXA1 expression was negatively correlated with the extent of its methylation, and its knockdown reduced proliferation, migration, and invasion, and induced G2/M phase arrest in HCT116 and SW480 cells by suppressing the phosphatase and tensin homolog/Akt signaling pathway and inhibiting epithelial–mesenchymal transition. Conclusion FOXA1 may act as an oncogene in colon cancer tumorigenesis and development.

scholarly journals Apigenin inhibits epithelial-mesenchymal transition of human colon cancer cells through NF-κB/Snail signaling pathway

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Jiafeng Tong ◽  
Ying Shen ◽  
Zhenghua Zhang ◽  
Ye Hu ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Human Colon ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Mesenchymal Transition ◽  
Human Colon Cancer Cells

Abstract Colon cancer is a leading cause of cancer-related deaths worldwide. The epithelial-mesenchymal transition (EMT) plays an important role in tumor metastasis of colon cancer. We first evaluated the effects of EMT-related transcription factors on the prognosis of colon cancer through analysis the data obtained from The Cancer Genome Atlas (TCGA). And then we screened a series of Chinese medicine monomers to find effect EMT inhibitors. First, Snail is a more important EMT transcription factors for colon cancer prognosis, compared with Twist and Slug. Then, we found that apigenin effectively inhibits the activity of Snail. Apigenin could inhibit the EMT, migration, and invasion of human colon cancer cells in vitro and in vivo through the NF-κB/Snail pathway. Snail is a key regulator of EMT in colon cancer and Snail inhibitor apigenin may be a therapeutic application for patients with colon cancer.

scholarly journals Cancer Preventive Effect of a Novel High Phenolic Sorghum Bran on Human Colon Cancer Cells (P05-008-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Seong-Ho Lee ◽  
Jihye Lee ◽  
Thomas Herald ◽  
Sarah Cox ◽  
Leela Noronha ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Citric Acid ◽  
Cancer Cells ◽  
Human Colon ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Sorghum Bran ◽  
Human Colon Cancer Cells

Abstract Objectives Colon cancer is one of leading causes of cancer mortality worldwide. Sorghum is the fifth most largely cultivated crop for human diet in the world. Most sorghum varieties contain high content of phenolic compounds. The objective of the current study is to evaluate the anti-cancer properties of a novel high phenolic sorghum bran extract prepared under 70% ethanol with 5% citric acid solvent. Methods High phenolic sorghum, accession number PI570481, was grown in Puerto Vallarta, Mexico winter nursery during the 2018 and high phenolic sorghum bran extract was prepared using 70% ethanol with 5% citric acid solvent at room temperature for 2 hours. Human colon cancer cell lines (HCT15, SW480, HCT116 and HT-29) were treated with different doses of high phenolic sorghum bran extract. Cell proliferation and apoptosis was measured using MTS assay and Alexa Fluor 488 Annexin V/Dead Cell Apoptosis system, respectively. Distribution of cell cycle was measured Texas Red channel using BD LSRFortessa system. Cell migration and invasion was measured using wound healing assay and Matrigel, respectively. The luciferase activity of reporter genes was measured using a dual-luciferase assay and Western blot was performed to measure expression of cancer phenotype-associated proteins. Results Cell proliferation was inhibited and apoptosis was induced in the human colon cancer cells treated with high phenolic sorghum bran extract in a dose-dependent manner. High phenolic sorghum bran extract led to S phage arrest. Cell migration and invasion was also repressed in the human colon cancer cells treated with high phenolic sorghum bran extract. The change of cancer phenotypes was associated with up- or down-regulation of regulatory genes. Conclusions The present study expands our understanding on the potential use of high phenolic sorghum bran for prevention of human colon cancer. Funding Sources Cooperative Agreement grant from USDA-ARS to S-HL.

Alterations of O-glycan biosynthesis in human colon cancer tissues

Glycobiology ◽  
1994 ◽  
Vol 4 (6) ◽  
pp. 873-884 ◽  
Author(s):  
Ji-Mao Yang ◽  
James C. Byrd ◽  
Bader B. Siddiki ◽  
Yong-Suk Chung ◽  
Masahiro Okuno ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Cancer Tissues

scholarly journals Wnt5a promotes human colon cancer cell migration and invasion but does not augment intestinal tumorigenesis in Apc 1638N mice

2013 ◽  
Vol 34 (11) ◽  
pp. 2629-2638 ◽  
Author(s):  
Elvira R.M. Bakker ◽  
Asha Mooppilmadham Das ◽  
Werner Helvensteijn ◽  
Patrick F. Franken ◽  
Sigrid Swagemakers ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Intestinal Tumorigenesis

scholarly journals cis-Golgi resident proteins and O-glycans are abnormally compartmentalized in the RER of colon cancer cells

1993 ◽  
Vol 105 (3) ◽  
pp. 819-830 ◽  
Author(s):  
G. Egea ◽  
C. Franci ◽  
G. Gambus ◽  
T. Lesuffleur ◽  
A. Zweibaum ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Golgi Apparatus ◽  
Cancer Cells ◽  
Neoplastic Transformation ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Normal Colon ◽  
Human Colon Cancer ◽  
Protein Disulphide Isomerase ◽  
Cancer Tissues

Neoplastic transformation is commonly associated with altered glycosylation of proteins and lipids. To understand the basis for altered mucin glycosylation, we have examined the distribution of RER markers, a cis-Golgi resident protein, and the GalNAc alpha-O-Ser/Thr epitope (Tn) in human colon cancer cells and in normal colon. In cultured mucin-producing colon cancer cells, Gal-NAc alpha-O-Ser/Thr was found in mucin droplets and in RER cisternae. In addition, the Golgi apparatus was disorganized in a proportion of cells and a 130 kDa cis-Golgi resident protein was also abnormally redistributed to the RER. The distribution of the MUC2 intestinal apomucin, protein disulphide isomerase, Gal-NAc alpha-O-Ser/Thr, and the 130 kDa cis-Golgi resident protein was analysed in normal colon and in colon cancer tissues. In normal colon, MUC2 apomucin and protein disulphide isomerase were located in the RER, whereas the cis-Golgi resident protein and GalNAc alpha-O-Ser/Thr were detected only in the cis-Golgi compartment. In contrast, the two Golgi markers colocalized with the MUC2 apomucin and protein disulphide isomerase in the RER of colon cancer cells. On the basis of these results, we propose that in colon cancer cells a redistribution of molecules normally present in the Golgi apparatus takes place; this alteration may contribute to the abnormal glycosylation of proteins and lipids associated with neoplastic transformation.

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