| A possible tumor suppressor role of the KLF5 transcription factor in human breast cancer. | breast, |
| Gene deletion and loss of expression and cell growth suppression indicate that KLF5 may be tumor suppressor gene at 13q21 in prostate cancer. Mutation and promoter methylation do not commonly inactivate KLF5 in prostate cancer. | prostate, |
| deacetylation switched KLF5 to tumor promoting activity, and blocking TGFbeta signaling attenuated the tumor suppressor activity of KLF5 | None |
| Data demonstrate that KLF5 inhibits ccRCC growth as a tumor suppressor and highlight the potential of 5-Aza-CdR to release KLF5 expression as a therapeutic modality for the treatment of ccRCC. | None |
| KLF5 may play an oncogenetic role in gastric carcinogenesis. | gastric, |
| Identification of small-molecule inhibitors of the colorectal cancer oncogene Kruppel-like factor 5 expression by ultrahigh-throughput screening. | colorectal, |
| Results argue that KLF5 acts as a fundamental core regulator of intestinal oncogenesis at the stem-cell level, and they suggest KLF5 targeting as a rational strategy to eradicate stem-like cells in colorectal cancer. | colorectal, |
| Klf5 deletion promotes Pten deletion-initiated luminal-type mouse prostate tumors through multiple oncogenic signaling pathways. | prostate, |
| KLF5 as an essential factor required for acinar-to-ductal metaplasia and oncogenic KRAS-induced pancreatic tumor formation. | pancreatic, |
| KLF5 recruited p300 to the RP1 promoter to enhance RP1 expression and regulated RP1 plays an oncogenic role in breast cancer by suppressing p27kip1. | breast, |
| Positive and negative regulation of the cardiovascular transcription factor KLF5 by p300 and the oncogenic regulator SET through interaction and acetylation on the DNA-binding domain. | None |
| KLF5 mediates the transforming effect of oncogenic H-Ras in NIH3T3 fibroblast cells and does so by transactivating the cyclin D1 promoter | None |
| increased expression of KLF5 in H-Ras-transformed cells is secondary to increased MAPK activity from H-Ras overexpression and that the elevated level of KLF5 is in part responsible for the proproliferative and transforming activities of oncogenic H-Ras. | None |
| This study reports that KLF5 is activated by oncogenic HRAS and that activated KLF5 promotes mitosis by inducing transcription of the cyclin B1 and Cdc2 genes. | None |