Genistein induces Gadd45 gene and G2/M cell cycle arrest in the DU145 human prostate cancer cell line.

Genistein is the most abundant isoflavone of soybeans and has been shown to cause growth arrest in various human cancer cell lines. However, the precise mechanism for this is still unclear. We report here that the growth arrest and DNA damage-inducible gene 45 (gadd45) gene is induced by genistein via its promoter in a DU145 human prostate cancer cell line.

Histone deacetylase inhibitors -Promising agents for 'gene-regulating chemoprevention' and 'molecular-targeting prevention' of cancer-.

One of the best approaches against cancer is prevention. Inactivation of the p53 or p16(INK4a) genes has been extensively reported in most human cancer cells. Both p53 and p16(INK4a) function as tumor suppressors.

p53-independent induction of Gadd45 by histone deacetylase inhibitor: coordinate regulation by transcription factors Oct-1 and NF-Y.

Histone deacetylase (HDAC) inhibitors cause growth arrest at the G1 and/or G2/M phases, and induce differentiation and/or apoptosis in a wide variety of tumour cells. The growth arrest at G1 phase by HDAC inhibitors is thought to be highly dependent on the upregulation of p21/WAF1, but the precise mechanism by which HDAC inhibitors cause G2/M arrest or apoptosis in tumour cells is unknown. Gadd45 causes cell cycle arrest at the G2/M phase transition and participates in genotoxic stress-induced apoptosis.

15-Deoxy-Delta(12,14)-prostaglandin J2 induces apoptosis through activation of the CHOP gene in HeLa cells.

Cyclopentenone prostaglandins (PGs) of the J series, which are produced by dehydration of PGD(2), have been reported to induce apoptosis in various cell lines. One of these cyclopentenone PGs, 15-deoxy-Delta(12,14)-prostaglandin J(2) (15-d-PGJ(2)), is the most potent inducer of apoptosis in the series, but the signaling pathways by which it induces apoptosis are poorly understood. We recently reported that cyclopentenone PGs accumulate in the endoplasmic reticulum (ER) and it has been shown that the transcription factor CHOP is induced by ER-stresses and elicits apoptosis.