Investigators demonstrated that the PARP inhibitor 123I-MAPi was a viable agent for the systemic administration and treatment of p53 mutant cancers. p53+/+ and p53–/– human colorectal cancer cell lines were evaluated for the ability of 123I-MAPi to induce tumor growth delay.
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B-Myb overexpression accelerated cell proliferation, cell cycle progression and cell motility in colorectal cancer cells, and promoted tumor growth in orthotopic nude mouse models in vivo.
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The authors explain how different metabolites of tryptophan are involved in the pathophysiology of inflammatory bowel disease (IBD) and colorectal cancer, as a major complication of IBD.
[International Reviews of Immunology]
Colorectal cancer cells hijacked prostaglandin E2 (PGE2) to non-canonically promote Hedgehog transcriptional factor Gli activity and Gli-dependent proliferation of colorectal cancer cells in a Smo-independent manner.
[Cell Death & Disease]
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Scientists characterized cetuximab and panitumumab exposure influence on miR expression in colorectal cancer cells to identify those regulating the EGFR pathway and implicated in resistance to treatment.
[Biomarkers in Medicine]
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The authors described the role of the long non-coding RNA SPRY4 intronic transcript 1 (SPRY4-IT1) in cancer metastasis by mechanisms related to Staufen1-mediated mRNA decay, and found that high SPRY4-IT1 expression was associated with aggressiveness and poor outcome in human colorectal, breast and ovarian cancer tissues.
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Scientists evaluated the effects of Bryophytes like Abietinella abietina, Homolothecium sericeum, Tortella tortuosa, Syntrichia ruralis, and Bryoerythrophyllum rubrum species extracted with ethyl alcohol on 5-fluorouracil resistant colorectal cancer cell lines.
[Nutrition and Cancer-An International Journal]
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The authors determined that 14-3-3σ expression was significantly downregulated in primary human colorectal cancer when compared with adjacent normal colonic tissue in patient samples. Downregulation of 14-3-3σ in primary colorectal cancers was significantly associated with p53 mutation, increasing tumor stage, distant metastasis, and poor patient survival.
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The authors investigated the mechanisms by which PRDX2 promoted the proliferation of colorectal cancer, and found that the oncogenic property of PRDX2 may have been attributed to its regulation of the RPL4-MDM2-p53 pathway, leading to p53 ubiquitinated degradation.
[Cell Death & Disease]
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The clustering of integrin α5ß1 at the plasma membrane of colorectal cancer-derived epithelial cells modulated their ability to respond to stimulation by receptor tyrosine kinase-activating growth factors EGF, NRG and HGF, through GSK3-mediated suppression of Akt pathway.
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The effects of worenine on colorectal cancer cell proliferation, colony formation and cell cycle distribution were measured.
[Cellular & Molecular Biology Letters]
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