RESUMO
Prostate cancer is one of the most common diseases in men worldwide. Surgery, radiation therapy, and hormonal therapy are effective treatments for early-stage prostate cancer. However, the development of castration-resistant prostate cancer has increased the mortality rate of prostate cancer. To develop novel drugs for castration-resistant prostate cancer, the molecular mechanisms of prostate cancer progression must be elucidated. Among the signaling pathways regulating prostate cancer development, recent studies have revealed the importance of noncanonical wingless-type MMTV integration site family (WNT) signaling pathways, mainly that involving WNT5A, in prostate cancer progression and metastasis; however, its role remains controversial. Moreover, chromatin remodelers such as the switch/sucrose nonfermentable (SWI/SNF) complex and chromodomain helicase DNA-binding proteins 1 also play important roles in prostate cancer progression through genome-wide gene expression changes. Here, we review the roles of noncanonical WNT signaling pathways, chromatin remodelers, and epigenetic enzymes in the development and progression of prostate cancer.
Assuntos
Masculino , Humanos , Via de Sinalização Wnt , Cromatina , Neoplasias de Próstata Resistentes à Castração , Montagem e Desmontagem da CromatinaRESUMO
Ovarian cancer is the most malignant gynecologic malignancy. In recent years, histone modifying enzymes (HMEs) have been widely studied as an important part of epigenetic modifi-cations in ovarian cancer. Histone modifying enzymes, including histone methyltransferases and demethylases, histone acetyltransferases and deacetylases, play an important role in the prolif-eration and migration of ovarian cancer cells by modifying histone and non-histone proteins, and can regulate the development of chemoresistance. Inhibitors of various histone modifying enzymes play good anti-tumor effects in ovarian cancer by promoting cell growth arrest and apoptosis, inhibi¬ting tumor cell invasion, and increasing chemo¬therapy sensitivity, and are expected to be a new strategy for precision treatment of ovarian cancer. Therefore, this paper will review the mechanism of action and therapeutic potential of histone modifying enzymes involved in methylation and acetylation processes in ovarian cancer.
RESUMO
Objective To investigate the synergistic regulation of KDM3B and JMJD1C in leukemia. Methods The expression level of JMJD1C and KDM3B were analyzed in multiple acute myeloid leukemia (AML) cell lines. AML cell lines NB4 and HL-60 were treated with Daminozide, followed by determination of H3K9 mono-methylation and di-methylation. AML cell lines NB4 and HL-60 were treated with Daminozide, ATRA (retinoid acid All-trans), C Vitamin and the expression of KDM3B and JMJD1C were detected by real-time quantitative PCR. Results The expression level of KDM3B and JMJD1C in the AML cell lines was negatively correlated. In NB4 and HL-60 cells treated by daminozide, H3K9 mono-methylation and di- methylation level showed a rising trend in these two cell groups. After treatment of NB4 cells with the 3 reagents, the level of mRNA of KDM3B was down-regulated while the level of mRNA of JMJD1C was up-regulated. In HL-60 cells treated by daminozide, the mRNA level of KDM3B was up-regulated and the mRNA level of JMJD1C was down-regulated. Conclusion The expression of KDM3B and JMJD1C is negatively correlated in patients with AML.