The zinc-finger transcription factor Klf4 is required for normal gastric epithelial proliferation and differentiation in vivo

Krüppel-like factor 4 exhibits antiapoptotic activity following γ-radiation-induced DNA damage

“…Mouse embryo fibroblasts derived from Klf4-null embryos are highly susceptible to apoptosis following DNA damage To further confirm the results obtained from RKO and HCT116 cells, both of which are cancerous, we investigated the response of mouse embryo fibroblasts (MEFs) derived from embryos that are WT ( þ / þ ) or null (À/À) for the Klf4 alleles (Katz et al, 2002). As shown in Figure 5a, Klf4 À/À MEFs were highly prone to g-radiation-induced apoptosis as compared to Klf4 þ / þ MEFs.…”

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

“…Current studies in carcinogen-esis have revealed that KLF4 can function as both tumor promoter and tumor suppressor depending on tissue type and cellular context [241]. The oncogenic effect of KLF4 has been reported in breast and squamous cell carcinoma [243][244][245][246][247], while its tumor suppression role was reported in various types of cancers such as colon cancer [248,249]. It was demonstrated that KLF4 is a fast turnover protein, whose turnover-half life is governed by the ubiquitin-proteasome system [250,251].…”

KLF4, p21 and context-dependent opposing forces in cancer

“…For example, mice deficient for one of multiple components of the Notch pathway develop an increased number of secretory cells, including goblet cells 119,120 , whereas activation of the Notch pathway results in a complete lack of development of goblet cells 121,122 . KLF4 deficiency, on the other hand, results in the production of fewer goblet cells 30 and a drop in p21 protein levels 37 . Besides causing a reduction in levels of KLF4 expression, loss of APC results in fewer goblet cells 123 .…”

“…CDKN1A, are involved in differentiation and cell-cycle inhibition 28 (TABLE 1). Klf4-knockout mice show defects in skin differentiation 29 as well as a reduced number of secretory goblet cells in the colon 30 , indicating that KLF4 functions as a proliferation-differentiation switch. Loss of KLF4-mediated terminal differentiation might therefore pave the way for unscheduled cellular proliferation.…”