<i>Conclusion</i>: ZEB2-AS1 could promote colon cancer cell proliferation and inhibit apoptosis to promote the progression of colon cancer by upregulating the expression of β-catenin protein.
<i>In vitro</i>, LINC00959 knockdown enhanced colon cancer cell proliferation, invasion, and migration; upregulated N-cadherin and vimentin; and downregulated E-cadherin and Caspase-3.
<i>In vivo</i> biodistribution and imaging studies were performed with positron emission tomography and magnetic resonance imaging (PET/MRI) studies to identify and quantitate <sup>89</sup>Zr-DS-5573a tumor uptake in a B7-H3-positive breast cancer model (MDA-MB-231) and a B7-H3-negative murine colon cancer model (CT26).
<i>In vivo</i> biodistribution and imaging studies were performed with positron emission tomography and magnetic resonance imaging (PET/MRI) studies to identify and quantitate <sup>89</sup>Zr-DS-5573a tumor uptake in a B7-H3-positive breast cancer model (MDA-MB-231) and a B7-H3-negative murine colon cancer model (CT26).
<i>L. acidophilus</i> and <i>B. bifidum</i> probiotics with the modification of the biochemical parameters and the expression of the VDR and LPR genes can play a key role in the protection of mouse colon cancer.
<i>L. acidophilus</i> and <i>B. bifidum</i> probiotics with the modification of the biochemical parameters and the expression of the VDR and LPR genes can play a key role in the protection of mouse colon cancer.
<i>Lycium barbarum</i> Polysaccharide Promotes Maturation of Dendritic Cell via Notch Signaling and Strengthens Dendritic Cell Mediated T Lymphocyte Cytotoxicity on Colon Cancer Cell CT26-WT.
<i>NAMPT</i> Is a Potent Oncogene in Colon Cancer Progression that Modulates Cancer Stem Cell Properties and Resistance to Therapy through Sirt1 and PARP.
<i>NAMPT</i> Is a Potent Oncogene in Colon Cancer Progression that Modulates Cancer Stem Cell Properties and Resistance to Therapy through Sirt1 and PARP.
<i>NAMPT</i> Is a Potent Oncogene in Colon Cancer Progression that Modulates Cancer Stem Cell Properties and Resistance to Therapy through Sirt1 and PARP.
(2) Among males, individuals who had MTHFRC677T T/T genotype were at a significantly higher risk of developing colon cancer (age-, residence-, smoking-, alcohol drinking-, tea consumption-adjusted OR=2.15, 95%CI: 1.07-4.33) compared with those who had C677T C allele.
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma).
(i) FN from fetal connective tissue, placenta, amniotic fluid, hepatoma, and colon carcinoma as well as cell lines from fetal tissues (WI-38), hepatomas (HuH-6 and HuH-7), and sarcoma (VA13) was characterized by the presence of the FDC-6-defined domain and by a high molecular weight (subunit Mr, 310,000-335,000).
- ARID1A-deficient EACs show a phenotype similar to colon cancer with high microsatellite instability but do not appear to have any prognostic significance.
1,1-Bis(3'-indolyl)-1-(p-substitutedphenyl)methanes are peroxisome proliferator-activated receptor gamma agonists but decrease HCT-116 colon cancer cell survival through receptor-independent activation of early growth response-1 and nonsteroidal anti-inflammatory drug-activated gene-1.
1,1-Bis(3'-indolyl)-1-(p-substitutedphenyl)methanes are peroxisome proliferator-activated receptor gamma agonists but decrease HCT-116 colon cancer cell survival through receptor-independent activation of early growth response-1 and nonsteroidal anti-inflammatory drug-activated gene-1.