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Butyrate Activates the WAF1/Cip1 Gene Promoter through Sp1 Sites in a p53-negative Human Colon Cancer Cell Line*
It is suggested that butyrate arrests the growth of WiDr by activating the WAF1/Cip1 promoter through specific Sp1 sites in a p53-independent fashion.
Aromatic hydrocarbon receptor-driven Bax gene expression is required for premature ovarian failure caused by biohazardous environmental chemicals
Oocytes in human ovarian biopsies grafted into immunodeficient mice also accumulate Bax and undergo apoptosis after PAH exposure in vivo, indicating that Ahr-driven Bax transcription is a novel and evolutionarily conserved cell-death signaling pathway responsible for environmental toxicant-induced ovarian failure.
Histone deacetylase inhibitor activates the WAF1/Cip1 gene promoter through the Sp1 sites.
Results demonstrate that transcriptional activation through the Sp1 sites of the WAF1/Cip1 promoter by TSA coincides with induced hyperacetylation of histone H4.
Antitumor activities of JTP-74057 (GSK1120212), a novel MEK1/2 inhibitor, on colorectal cancer cell lines in vitro and in vivo.
- Takayuki Yamaguchi, Reina Kakefuda, N. Tajima, Y. Sowa, T. Sakai
- Biology, MedicineInternational journal of oncology
- 1 July 2011
Results suggest the usefulness of JTP-74057 in therapeutic applications for colorectal cancer patients and its antitumor activities in vitro and in vivo, and sensitivity was enhanced by an Akt inhibitor.
Thioredoxin-dependent Redox Regulation of p53-mediated p21 Activation*
TRX-dependent redox regulation of p53 activity indicates coupling of the oxidative stress response and p53-dependent repair mechanism.
Hes1 Directly Controls Cell Proliferation through the Transcriptional Repression of p27Kip1
The results have suggested that Hes1 directly contributes to the promotion of progenitor cell proliferation through transcriptional repression of a cyclin-dependent kinase inhibitor, p27Kip1.
Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells
It is shown for the first time that the apoptosis by luteolin is mediated through death receptor 5 (DR5) upregulation, and the possibility that treatment with luteolini might be promising as a new therapy against cancer is raised.
Allele-specific hypermethylation of the retinoblastoma tumor-suppressor gene.
- T. Sakai, J. Toguchida, N. Ohtani, D. Yandell, J. Rapaport, T. Dryja
- Biology, MedicineAmerican journal of human genetics
- 22 May 1991
It is believed that the hypermethylation of the retinoblastoma gene that is found in these tumors corresponds to the allelic inactivation of the gene, and it is speculated that erroneous hyperethylation without alteration of nucleotide sequence occasionally plays a role in the genesis of this cancer.
Histone deacetylase inhibitors upregulate death receptor 5/TRAIL-R2 and sensitize apoptosis induced by TRAIL/APO2-L in human malignant tumor cells
- Susumu Nakata, Tatsushi Yoshida, M. Horinaka, T. Shiraishi, M. Wakada, T. Sakai
- Biology, ChemistryOncogene
- 19 August 2004
Death receptor 5 (DR5) is a receptor for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). TRAIL is a promising candidate for cancer therapeutics due to its ability to induce apoptosis…
Activation of the p21WAF1/CIP1 promoter independent of p53 by the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) through the Sp1 sites
SAHA activates the p21 promoter through the Sp1 sites, and that both Sp1 and Sp3 proteins can mediate SAHA-induced gene activation, which suggests that SAHA induces cell cycle arrest and apoptosis in human breast cancer cells via a p53-independent mechanism.