期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 26, 期 22, 页码 8418-8426出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00821-06
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资金
- Medical Research Council [G0301154] Funding Source: researchfish
- Medical Research Council [G0301154] Funding Source: Medline
- MRC [G0301154] Funding Source: UKRI
Inhibition of the mutationally activated Wnt cascade in colorectal cancer cell lines induces a rapid G(1) arrest and subsequent differentiation. This arrest can be overcome by maintaining expression of a single Tcf4 target gene, the proto-oncogene c-Myc. Since colorectal cancer cells share many molecular characteristics with proliferative crypt progenitors, we have assessed the physiological role of c-Myc in adult crypts by conditional gene deletion. c-Myc-deficient crypts are lost within weeks and replaced by c-Myc-proficient crypts through a fission process of crypts that have escaped gene deletion. Although c-Myc(-/-) crypt cells remain in the cell cycle, they are on average much smaller than wild-type cells, cycle slower, and divide at a smaller cell size. c-Myc appears essential for crypt progenitor cells to provide the necessary biosynthetic capacity to successfully progress through the cell cycle.
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