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Chromodomain helicase DNA binding protein 5 (CHD5) has been identified as a tumor suppressor in mouse models. Downregulation of CHD5 gene expression is frequently observed in breast cancer cells and tissues. This may be explained by deletions or other mutations; however, alternative mechanisms require investigation. Therefore, the present study evaluated whether CHD5 aberrant methylation has a role in primary breast tumors. A total of 389 patients with primary breast cancer (including 252 paraffin-embedded specimens and 137 fresh-frozen samples) were enrolled in the present study. In the current study, reverse transcription-polymerase chain reaction (RT-PCR) and nested-methylation-specific PCR were used to analyze the mRNA expression and promoter methylation of CHD5 genes in a large cohort of breast cancer patients, and to investigate their associations with the clinicopathological features of tumors. CHD5 expression was significantly suppressed in breast cancer tissues compared with normal breast tissues when analyzed by RT-PCR. Furthermore, DNA methylation of CHD5 was more prevalent in breast tumors than in normal tissues. CHD5 mRNA levels correlated with the degree of CHD5 methylation in breast cancer tissues. Clinicopathological correlation analysis revealed that CHD5 promoter methylation was associated with estrogen receptor and progesterone receptor status. Thus, downregulation of CHD5, mediated by abnormal methylation, may contribute to the development and progression of breast cancer. [ABSTRACT FROM AUTHOR]

Isatin has been shown to initiate apoptotic processes in SH-SY5Y neuroblastoma cells. The aim of the present study was to investigate whether isatin is also able to alter the proliferation and migratory ability of SH-SY5Y cells. The results demonstrated that the proportion of SH-SY5Y cells in G1 phase was significantly increased following treatment with isatin for 48 h with simultaneous downregulation of cyclin D1 expression. In addition, isatin significantly inhibited cell migration and invasion, along with decreases in matrix metalloproteinase (MMP)2 and MMP9 expression. In addition, isatin reduced the levels of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in a concentration-dependent manner. These results demonstrated that isatin induces G1-phase arrest in SH-SY5Y cells, possibly by decreasing cyclin D1 expression as well as inhibiting their migration and invasiveness, probably by reducing MMP2 and MMP9. These effects may be exerted by isatin via a downregulating the levels of pSTAT3. [ABSTRACT FROM AUTHOR]